Showing papers in "Bioengineered bugs in 2021"

A critical review on advances in the practices and perspectives for the treatment of dye industry wastewater.

Abstract: Rapid industrialization has provided comforts to mankind but has also impacted the environment harmfully. There has been severe increase in the pollution due to several industries, in particular due to dye industry, which generate huge quantities of wastewater containing hazardous chemicals. Although tremendous developments have taken place for the treatment and management of such wastewater through chemical or biological processes, there is an emerging shift in the approach, with focus shifting on resource recovery from such wastewater and also their management in sustainable manner. This review article aims to present and discuss the most advanced and state-of-art technical and scientific developments about the treatment of dye industry wastewater, which include advanced oxidation process, membrane filtration technique, microbial technologies, bio-electrochemical degradation, photocatalytic degradation, etc. Among these technologies, microbial degradation seems highly promising for resource recovery and sustainability and has been discussed in detail as a promising approach. This paper also covers the challenges and future perspectives in this field.

Antibiotics: An overview on the environmental occurrence, toxicity, degradation, and removal methods.

Abstract: Antibiotics, as antimicrobial drugs, have been widely applied as human and veterinary medicines. Recently, many antibiotics have been detected in the environments due to their mass production, widespread use, but a lack of adequate treatment processes. The environmental occurrence of antibiotics has received worldwide attention due to their potential harm to the ecosystem and human health. Research status of antibiotics in the environment field is presented by bibliometrics. Herein, we provided a comprehensive overview on the following important issues: (1) occurrence of antibiotics in different environmental compartments, such as wastewater, surface water, and soil; (2) toxicity of antibiotics toward non-target organisms, including aquatic and terrestrial organisms; (3) current treatment technologies for the degradation and removal of antibiotics, including adsorption, hydrolysis, photodegradation and oxidation, and biodegradation. It was found that macrolides, fluoroquinolones, tetracyclines, and sulfonamides were most frequently detected in the environment. Compared to surface and groundwaters, wastewater contained a high concentration of antibiotic residues. Both antibiotics and their metabolites exhibited toxicity to non-target organisms, especially aquatic organisms (e.g., algae and fish). Fluoroquinolones, tetracyclines, and sulfonamides can be removed through abiotic process, such as adsorption, photodegradation, and oxidation. Fluoroquinolones and sulfonamides can directly undergo biodegradation. Further studies on the chronic effects of antibiotics at environmentally relevant concentrations on the ecosystem were urgently needed to fully understand the hazards of antibiotics and help the government to establish the permissible limits. Biodegradation is a promising technology; it has numerous advantages such as cost-effectiveness and environmental friendliness.

Naringenin alleviates myocardial ischemia/reperfusion injury by regulating the nuclear factor-erythroid factor 2-related factor 2 (Nrf2) /System xc-/ glutathione peroxidase 4 (GPX4) axis to inhibit ferroptosis.

Abstract: Ferroptosis is an important form of myocardial cell death in myocardial ischemia-reperfusion injury (MIRI). Naringenin (NAR), as a flavonoid, has a significant advantage in improving MIRI. But the regulatory effect and mechanism of NAR on ferroptosis in MIRI have not been reported. After the rats were given NAR and induced to form myocardial ischemia-reperfusion (MI/R) injury, Tetrazolium chloride (TTC) staining was used to detect the myocardial infarction area of rats, and Hematoxylin-eosin (H&E) staining was used to detect myocardial injury. The markers of tissue inflammation were detected by ELISA. Serum creatine kinase Serum creatin kinase (CPK), Lactate dehydrogenase (LDH), and lipid peroxide (LPO) and oxidative stress related levels were measured. In addition, iron detection kits were used to detect total iron and Fe2+ levels in cardiac tissues, and western blot was used to detect the expression of ferroptosis-related proteins and the expression of nuclear factor-erythroid factor 2-related factor 2 (Nrf2) and glutathione peroxidase 4 (GPX4). At the cellular level, H9C2 cardiomyocytes were induced by hypoxia/reoxygenation (H/R), and ferroptosis inducer Erastin was administered to detect cell viability, ferroptosis-related indicators, oxidative stress related indicators, and expressions of Nrf2 and GPX4, to explore the mechanisms involved. NAR alleviated MI/R-induced pathological damage, inflammation and lipid peroxidation in myocardial tissue of rats. NAR adjusted the NRF2 /System xc - /GPX4 axis and improved ferroptosis. At the cellular level, ferroptosis inducer Erastin reversed the protective effect of NAR on H/R-induced H9C2 cardiomyocytes. In conclusion, NAR can alleviate MIRI by regulating the Nrf2/System xc-/GPX4 axis to inhibit ferroptosis.

Apple orchard waste recycling and valorization of valuable product-A review

Abstract: Huge quantities of apple orchard waste (AOW) generated could be regarded as a promising alternative energy source for fuel and material production. Conventional and traditional processes for dispos...

A novel pyroptosis-related lncRNA signature for prognostic prediction in patients with lung adenocarcinoma.

Abstract: Lung adenocarcinoma (LUAD) has been the major cause of tumor-associated mortality in recent years and has a poor prognosis. Pyroptosis is regulated via the activation of inflammasomes and participates in tumorigenesis. However, the effects of pyroptosis-related lncRNAs (PRlncRNAs) on LUAD have not yet been completely elucidated. Therefore, we attempted to systematically explore patterns of cell pyroptosis to establish a novel signature for predicting LUAD survival. Based on TCGA database, we set up a prognostic model by incorporating PRlncRNAs with differential expression using Cox regression and LASSO regression. Kaplan-Meier analysis was conducted to compare the survival of LUAD patients. We further simplified the risk model and created a nomogram to enhance the prediction of LUAD prognosis. Altogether, 84 PRlncRNAs with differential expression were discovered. Subsequently, a new risk model was constructed based on five PRlncRNAs, GSEC, FAM83A-AS1, AL606489.1, AL034397.3 and AC010980.2. The proposed signature exhibited good performance in prognostic prediction and was related to immunocyte infiltration. The nomogram exactly forecasted the overall survival of patients and had excellent clinical utility. In the present study, the five-lncRNA prognostic risk signature and nomogram are trustworthy and effective indicators for predicting the prognosis of LUAD.

Ferrostatin-1 alleviates lipopolysaccharide-induced cardiac dysfunction.

Abstract: Cardiac dysfunction is a common complication of sepsis, and is attributed to severe inflammatory responses. Ferroptosis is reported to be involved in sepsis-induced cardiac inflammation. Therefore, we speculated that ferrostatin-1 (Fer-1), a ferroptosis inhibitor, improves cardiac dysfunction caused by sepsis. An intraperitoneal injection of lipopolysaccharide (LPS) was performed to induce a rat cardiac dysfunction model. Echocardiography, cardiac histopathology, biochemical and western blot results were analyzed. Twelve hours after the LPS injection, LPS-treated rats exhibited deteriorating cardiac systolic function, increased levels of cardiac injury markers and levels of ferroptosis markers prostaglandin endoperoxide synthase 2 (PTGS2). Additionally, LPS increased iron deposition in the myocardium, with downregulating ferroportin (FPN, SLC40A1) and transferrin receptor (TfR)expression, and upregulating ferritin light chain (FTL) and ferritin heavy chain (FTH1) expression. Meanwhile, LPS also increased lipid peroxidation in the rat heart by decreasing the expression of glutathione peroxidase 4 (GPX4). Moreover, the expression of inflammatory cytokines, such as tumor necrosis-alpha (TNF-α), interleukin-1 (IL-1β), and interleukin-6 (IL-6), and inflammatory cell infiltration were also increased following LPS challenge. Finally, the abovementioned adverse effects of LPS were relieved by Fer-1 except for TfR expression. Mechanistically, Fer-1 significantly reduced the levels of toll-like receptor 4 (TLR4), phospho-nuclear factor kappa B (NF-κB), and phospho-inhibitor of kappa Bα (IκBα) in LPS-treated rats. In summary, these findings imply that Fer-1 improved sepsis-induced cardiac dysfunction at least partially via the TLR4/NF-κB signaling pathway.

Interleukin-6 promotes ferroptosis in bronchial epithelial cells by inducing reactive oxygen species-dependent lipid peroxidation and disrupting iron homeostasis.

Abstract: Asthma occurs accompanied by the ferroptosis in bronchial epithelial cells, during which Interleukin-6 (IL-6) plays a key role. However, the associations between IL-6, ferroptosis and asthma have not been reported. Bronchial epithelial cells BEAS-2B cells were induced by different concentrations of IL-6 and cell viability was detected by MTT assay. The TBARS production rate was detected by corresponding kit. The expression of oxidative stress-related indexes was detected by ELISA. The Iron Assay Kits detected total iron levels and ferrous ion (Fe2+) levels. Labile iron pool assay was used to detect the cell unstable iron pool. The expression of ferroptosis-related proteins was detected by Western blot. To further examine the mechanism of action, ferroptosis inhibitor Ferrostatin 1 (Fer-1), antioxidant NAC, and the iron supplement Fe were added. We found that IL-6 decreased the activity, promoted lipid peroxidation, disrupted iron homeostasis of BEAS-2B cells, and induced iron death in bronchial epithelial BEAS-2B cells. However, pretreatment with Ferrostatin-1 (Fer-1) and antioxidant NAC partially reversed the effect of IL-6 on lipid peroxidation and ferroptosis in BEAS-2B cells, while Fe augmented the effect. Overall, IL-6 promotes ferroptosis in bronchial epithelial cells by inducing reactive oxygen species (ROS)-dependent lipid peroxidation and disrupting iron homeostasis.

Icariin alleviates osteoarthritis by regulating autophagy of chondrocytes by mediating PI3K/AKT/mTOR signaling.

Abstract: Osteoarthritis (OA) is a chronic degenerative disease that significantly impacts the quality of life of the elderly population. Recently, the pathogenesis of OA has been reported to involve autophagy in chondrocytes. Intriguingly, icariin, one of the main components of epimedium, exerts multiple pharmacological effects, including a protective effect against chondrocyte damage. Thus, we aimed to investigate the therapeutic effect of icariin on OA and its potential underlying mechanism by using a rat model of OA. After treatment with icariin or an autophagy activator (rapamycin) or inhibitor (3-methyladenine), OA chondrocyte viability was measured using the CCK-8 assay, apoptosis in the chondrocytes was evaluated using the acridine orange-propidium iodide assay and flow cytometry, and OA tissue pathological state was assessed using micro-CT scanning and safranin O staining. Furthermore, immunohistochemical staining was used to measure the expression level of Beclin-1 and immunofluorescence labeling was used to visualize LC3 expression, and western blotting was used to determine the expression levels of autophagy proteins and key proteins in the PI3K signaling pathway. The apoptotic rate of OA chondrocytes was markedly elevated by 3-methyladenine and suppressed by rapamycin and icariin; autophagy genes were drastically downregulated in the 3-methyladenine group and upregulated in the rapamycin and icariin groups; and the PI3K/AKT/mTOR signaling pathway was activated by 3-methyladenine and inhibited by rapamycin and icariin. Notably, following treatment with rapamycin and icariin, the severe pathological state in OA cartilage tissues was substantially alleviated, and this was accompanied by activated autophagy and inhibited PI3K signaling in the cartilage tissues. Taken together, these findings indicate that icariin alleviates OA by regulating the autophagy of chondrocytes by mediating PI3K/AKT/mTOR signaling.

The roles of microbial products in the development of colorectal cancer: a review

Abstract: A large number of microbes exist in the gut and they have the ability to process and utilize ingested food. It has been reported that their products are involved in colorectal cancer development. The molecular mechanisms which underlie the relationship between gut microbial products and CRC are still not fully understood. The role of some microbial products in CRC is particularly controversial. Elucidating the effects of gut microbiota products on CRC and their possible mechanisms is vital for CRC prevention and treatment. In this review, recent studies are examined in order to describe the contribution metabolites and toxicants which are produced by gut microbes make to CRC, primarily focusing on the involved molecular mechanisms.Abbreviations: CRC: colorectal cancer; SCFAs: short chain fatty acids; HDAC: histone deacetylase; TCA cycle: tricarboxylic acid cycle; CoA: cytosolic acyl coenzyme A; SCAD: short chain acyl CoA dehydrogenase; HDAC: histone deacetylase; MiR-92a: microRNA-92a; KLF4: kruppel-like factor; PTEN: phosphatase and tensin homolog; PI3K: phosphoinositide 3-kinase; PIP2: phosphatidylinositol 4, 5-biphosphate; PIP3: phosphatidylinositol-3,4,5-triphosphate; Akt1: protein kinase B subtype α; ERK1/2: extracellular signal-regulated kinases 1/2; EMT: epithelial-to-mesenchymal transition; NEDD9: neural precursor cell expressed developmentally down-regulated9; CAS: Crk-associated substrate; JNK: c-Jun N-terminal kinase; PRMT1: protein arginine methyltransferase 1; UDCA: ursodeoxycholic acid; BA: bile acids; CA: cholic acid; CDCA: chenodeoxycholic acid; DCA: deoxycholic acid; LCA: lithocholic acid; CSCs: cancer stem cells; MHC: major histocompatibility; NF-κB: NF-kappaB; GPR: G protein-coupled receptors; ROS: reactive oxygen species; RNS: reactive nitrogen substances; BER: base excision repair; DNA: deoxyribonucleic acid; EGFR: epidermal growth factor receptor; MAPK: mitogen activated protein kinase; ERKs: extracellular signal regulated kinases; AKT: protein kinase B; PA: phosphatidic acid; TMAO: trimethylamine n-oxide; TMA: trimethylamine; FMO3: flavin-containing monooxygenase 3; H2S: Hydrogen sulfide; SRB: sulfate-reducing bacteria; IBDs: inflammatory bowel diseases; NSAID: non-steroidal anti-inflammatory drugs; BFT: fragile bacteroides toxin; ETBF: enterotoxigenic fragile bacteroides; E-cadherin: extracellular domain of intercellular adhesive protein; CEC: colonic epithelial cells; SMOX: spermine oxidase; SMO: smoothened; Stat3: signal transducer and activator of transcription 3; Th17: T helper cell 17; IL17: interleukin 17; AA: amino acid; TCF: transcription factor; CDT: cytolethal distending toxin; PD-L1: programmed cell death 1 ligand 1.

Tumor-derived exosomal miRNA-141 promote angiogenesis and malignant progression of lung cancer by targeting growth arrest-specific homeobox gene (GAX).

Abstract: Previous researches have suggested that exosomal miRNA-141 has association with metastatic lung cancer, however, its role and regulatory mechanism require further study. In this study, exosomes were isolated from lung cancer patients and normal human serum and identified. We found that the expression of miRNA-141 was up-regulated in the lung cancer serum exosomes compared with the normal serum exosomes. When the exosomes were extracted for co-culture with HUVECs, they were absorbed and distributed around the nucleus by confocal microscopy. Moreover, exosomal miRNA-141 from A549 significantly not only promoted the migration and invasion of A549 but also increased the cell proliferation, tube formation of HUVECs. In order to reveal the mechanism of exosomal miRNA-141, bioinformatics analysis revealed that miRNA-141 targeted the binding of Growth arrest-specific homeobox gene (GAX) in the 3'UTR region, and confirmed by MS2-RIP assay and dual-luciferase assay. Exosome miRNA-141 could down-regulate the expression of GAX. Taken together, our results demonstrate that tumor-derived exosomal miRNA-141 promote angiogenesis and malignant progression of lung cancer by targeting GAX. It provides a new possibility for the treatment of lung cancer.

Production of polyhydroxyalkanoates (PHAs) by Bacillus megaterium using food waste acidogenic fermentation-derived volatile fatty acids.

Abstract: High production costs still hamper fast expansion of commercial production of polyhydroxyalkanoates (PHAs). This problem is greatly related to the cultivation medium which accounts for up to 50% of the whole process costs. The aim of this research work was to evaluate the potential of using volatile fatty acids (VFAs), derived from acidogenic fermentation of food waste, as inexpensive carbon sources for the production of PHAs through bacterial cultivation. Bacillus megaterium could assimilate glucose, acetic acid, butyric acid, and caproic acid as single carbon sources in synthetic medium with maximum PHAs production yields of 9-11%, on a cell dry weight basis. Single carbon sources were then replaced by a mixture of synthetic VFAs and by a VFAs-rich stream from the acidogenic fermentation of food waste. After 72 h of cultivation, the VFAs were almost fully consumed by the bacterium in both media and PHAs production yields of 9-10%, on cell dry weight basis, were obtained. The usage of VFAs mixture was found to be beneficial for the bacterial growth that tackled the inhibition of propionic acid, iso-butyric acid, and valeric acid when these volatile fatty acids were used as single carbon sources. The extracted PHAs were revealed to be polyhydroxybutyrate (PHB) by characterization methods of Fourier-transform infrared spectroscopy (FTIR) and differential scanning calorimetry (DSC). The obtained results proved the possibility of using VFAs from acidogenic fermentation of food waste as a cheap substrate to reduce the cost of PHAs production.

Circular RNA FAT atypical cadherin 1 (circFAT1)/microRNA-525-5p/spindle and kinetochore-associated complex subunit 1 (SKA1) axis regulates oxaliplatin resistance in breast cancer by activating the notch and Wnt signaling pathway.

Abstract: Increasing evidence has confirmed the vital roles of circular RNAs (CircRNAs) in the drug resistance of breast cancer (BC). Herein, we intended to study the effect of circular RNA FAT atypical cadherin 1 (circFAT1) on BC oxaliplatin (OX) resistance and find out the potential molecular mechanism in it. In this study, mRNA and protein levels of genes were measured by RT-qPCR and western blotting, respectively. Luciferase reporter assay confirmed the relationship between microRNA-525-5p (miR-525-5p) and circFAT1 or spindle and kinetochore-associated complex subunit 1 (SKA1). CCK-8, transwell, and flow cytometry experiments were utilized to investigate the chemosensitivity, migration, invasion, and apoptosis of BC cells. Gene Set Enrichment Analysis (GSEA) was applied to discover possible pathways related to SKA1. It was uncovered that circFAT1 was overexpressed in OX-resistant BC tissues and cells. Functional experiments showed that circFAT1 depletion reduced the level of chemoresistance-related genes. Moreover, circFAT1 knockdown remarkably facilitated apoptosis and decreased OX (half-maximal inhibitory concentration) IC50 value, migration, and invasion in OX-resistant BC cells. It was identified that miR-525-5p directly targeted circFAT1 and SKA1. Besides, rescue assays exhibited that circFAT1 promoted OX resistance in BC cells via the miR-525-5p/SKA1 regulatory network. Furthermore, GSEA and western blotting identified that SKA1 activated the Notch and Wnt pathway in OX-resistant BC cells. In conclusion, our results demonstrated that circFAT1 conferred OX resistance in BC by regulating the miR-525-5p/SKA1 via the Notch and Wnt pathway, providing a potential therapeutic target for patients with OX-resistant BC.

Physiology of microalgal biofilm: a review on prediction of adhesion on substrates.

Abstract: In view of high energy cost and water consumption in microalgae cultivation, microalgal-biofilm-based cultivation system has been advocated as a solution toward a more sustainable and resource friendlier system for microalgal biomass production. Algal-derived extracellular polymeric substances (EPS) form cohesive network to interconnect the cells and substrates; however, their interactions within the biofilm are poorly understood. This scenario impedes the biofilm process development toward resource recovery. Herein, this review elucidates on various biofilm cultivation modes and contribution of EPS toward biofilm adhesion. Immobilized microalgae can be envisioned by the colloid interactions in terms of a balance of both dispersive and polar interactions among three interfaces (cells, mediums and substrates). Last portion of this review is dedicated to the future perspectives and challenges on the EPS; with regard to the biopolymers extraction, biopolymers' functional description and cross-referencing between model biofilms and full-scale biofilm systems are evaluated. This review will serve as an informative reference for readers having interest in microalgal biofilm phenomenon by incorporating the three main players in attached cultivation systems: microalgae, EPS and supporting materials. The ability to mass produce these miniature cellular biochemical factories via immobilized biofilm technology will lay the groundwork for a more sustainable and feasible production.

Circular RNA circ_0001287 inhibits the proliferation, metastasis, and radiosensitivity of non-small cell lung cancer cells by sponging microRNA miR-21 and up-regulating phosphatase and tensin homolog expression

Abstract: As a type of non-coding RNA, circular RNA (circRNA) figures prominently in human cancer progression. Nonetheless, the expression, function, and regulatory mechanism of circ_0001287 in non-small cell lung cancer (NSCLC) remain obscure. In this work, quantitative real-time polymerase chain reaction (qRT-PCR) was implemented to quantify circ_0001287 and miR-21 expressions in NSCLC tissues and cells. The relationship between circ_0001287 expression and the clinicopathological parameters of NSCLC patients was examined. Cell counting kit-8 (CCK-8), 5-bromo-2©-deoxyuridine (BrdU), and Transwell experiments were conducted to detect the multiplication, migration, and invasion of NSCLC cells after circ_0001287 was overexpressed or knocked down. The survival of NSCLC cells was studied using colony formation experiment under different doses of radiation. RNA immunoprecipitation (RIP) experiment and luciferase reporter gene experiment verified the binding relationship between circ_0001287 and miR-21. Western blot was employed to examine the regulatory effects of circ_0001287 and miR-21 on phosphatase and tensin homolog (PTEN) expression. We reported that circ_0001287 expression was down-modulated in NSCLC tissues and cell lines. Besides, circ_0001287 low expression was associated with low differentiation and positive lymph node invasion of NSCLC. Circ_0001287 overexpression suppressed the multiplication, migration, invasion, and radioresistance of NSCLC cells, whereas circ_0001287 knockdown promoted the above phenotypes. Circ_0001287 could adsorb miR-21 and repress its expression, and indirectly up-modulate PTEN expression in NSCLC cells. Taken together, circ_0001287/miR-21/PTEN axis is probably involved in regulating NSCLC cell multiplication, metastasis, and radioresistance.

Long non-coding RNA H19 protects against intracerebral hemorrhage injuries via regulating microRNA-106b-5p/acyl-CoA synthetase long chain family member 4 axis.

Abstract: Intracerebral hemorrhage (ICH) is one of the most common refractory diseases. Long non-coding RNAs (lncRNAs) play crucial roles in ICH. This study was designed to investigate the role of lncRNA H19 in ICH and the underlying molecular mechanisms involved. Real-time quantitative polymerase chain reaction (RT-qPCR) was performed to determine mRNA expression. Cell viability was analyzed using Cell Counting Kit 8 (CCK8). PI staining Flow cytometry and TdT-mediated biotinylated nick end-labeling (TUNEL) assays were performed to determine ferroptosis in brain microvascular endothelial cells (BMVECs). Targeting relationships were predicted using Starbase and TargetScan and verified by RNA pull-down and luciferase reporter gene assays. Western blotting was performed to assess protein expression. LncRNA H19 is highly expressed in ICH model cells. Over-expression of H19 suppressed cell viability and promoted ferroptosis of BMVECs. miR-106b-5p is predicted to be a target of H19. The expression of miR-106b-5p was lower in oxygen and glucose deprivation hemin-treated (OGD/H-treated) cells. Over-expression of miR-106b-5p reversed the effects of H19 on cell viability and ferroptosis in BMVECs. Furthermore, acyl-CoA synthetase long-chain family member 4 (ACSL4) was verified to be a target gene of miR-106b-5p and was highly expressed in OGD/H-treated cells. Upregulation of ACSL4 inhibited the effects of miR-106b-5p and induced BMVEC dysfunction. In conclusion, lncRNA H19 was overexpressed in ICH. Knockdown of H19 promoted cell proliferation and suppressed BMVECs ferroptosis by regulating the miR-106b-5p/ACSL4 axis. Therefore, H19 knockdown may be a promising therapeutic strategy for ICH.

Transferrin receptor-mediated reactive oxygen species promotes ferroptosis of KGN cells via regulating NADPH oxidase 1/PTEN induced kinase 1/acyl-CoA synthetase long chain family member 4 signaling.

Abstract: Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women of reproductive age. Abnormal ovarian folliculogenesis is the main factor responsible for PCOS. Iron metabolism plays a vital role in endocrine disorder. This study aimed to investigate the potentials of iron metabolism in PCOS and the underlying molecular mechanisms. Mice were injected with dehydroepiandrosterone (DHEA) to establish the PCOS model in-vivo. H & E staining was performed for histological analysis; qRT-PCR and western blot were employed to determine the mRNA and protein expressions. Immunofluorescence was used for mitochondrial staining. Cellular functions were detected using CCK-8 and PI staining assays. Ferric ammonium citrate (FAC) activates the transferrin receptor (TFRC), increases the iron content, and suppresses the cell viability of the human granulosa-like tumor cell line (KGN). However, TFRC knockdown suppressed ferroptosis of KGN cells. Iron uptake mediated the activation of NADPH oxidase 1 (NOX1) signaling, which induced the release of reactive oxygen species (ROS) and mitochondrial damage. Moreover, TFRC activated PTEN induced kinase 1 (PINK1) signaling and induced mitophagy; iron-uptake-induced upregulation of acyl-CoA synthetase long chain family member 4 (ACSL4) was required for mitophagy activation and glutathione peroxidase 4 (GPX4) degradation. Additionally, FAC increased iron uptake and suppressed the folliculogenesis in-vivo. In conclusion, TFRC increased the iron content, mediated the release of ROS, activated mitophagy, and induced lipid peroxidation, which further promoted the ferroptosis of KGN cells. Therefore, the inhibitory effects of TFRC/NOX1/PINK1/ACSL4 signaling on folliculogenesis can be a potential target for PCOS.[Figure: see text].

Long non-coding RNA (LncRNA) MRPL23-AS1 promotes tumor progression and carcinogenesis in osteosarcoma by activating Wnt/β-catenin signaling via inhibiting microRNA miR-30b and upregulating myosin heavy chain 9 (MYH9).

Abstract: Long non-coding RNA (LncRNA) contributes to the occurrence and development of osteosarcoma (OS), although the underlying mechanism is not clear. In the present study, we showed that lncRNA MRPL23-AS1 was remarkably increased in OS tissues and cell lines. Stable knockdown of MRPL23-AS1 evidently attenuated cell viability and invasive ability, meanwhile inhibited in vivo tumor growth and dissemination. In terms of mechanism, luciferase reporter, RNA pull-down and fluorescence in situ hybridization (FISH) assays showed that MRPL23-AS1 competitively interacted with miR-30b, increasing myosin heavy chain 9 (MYH9) expression, a trans- activator of β-catenin, resulting in the activation of Wnt/β-catenin pathway, thereby promoting OS tumorigenesis and metastasis. Importantly, high MRPL23-AS1 was positively correlated with MYH9, while conversely correlated with miR-30b, suggesting that the regulatory axis of MRPL23-AS1/miR-30b/MYH9 does exist in OS. Clinically, OS patients with high MRPL23-AS1 had larger tumor size, higher stage and easier metastasis than those with low MRPL23-AS1, moreover, MRPL23-AS1 was identified as an adverse prognostic factor for OS survival. In conclusion, our results show that MRPL23-AS1 is a key oncogenic lncRNA in OS, targeting of MRPL23-AS1 may be a promising treatment for OS patients.

Diatom microalgae as smart nanocontainers for biosensing wastewater pollutants: Recent trends and innovations.

Abstract: Microalgae have been recognized as one of the most efficient microorganisms to remediate industrial effluents. Among microalgae diatoms are silica shelled unicellular eukaryotes, found in all types of water bodies and flourish very well even in wastewater. They have their silica cell wall made up of nano arrayed pores arranged in a similar fashion. Therefore, they act as smart nanocontainers to adsorb various trace metals, dyes, polymers and drugs which are hazardous to human as well to aquatic life. The beautiful nanoarchitecture in diatoms allows them to easily bind to ligands of choice to form a nanocomposite structure with the pollutants. Such naturally available nanomaterials are economical and highly sensitive compared to manmade artificial silica nanotubes to easily remove the toxic pollutants from wastewater. This review is focused on employing diatom microalgae to remediate various pollutants such as heavy metals, dyes, hydrocarbons detected in the wastewater. It also includes different microalgae as biosensors for determination of pollutants in effluents and the perspectives for nanotechnological applications in the field of remediating pollutants through microalgae. The review also discusses in length the hurdles and perspectives of employing microalgae in wastewater remediation.

Analysis of Collagen type X alpha 1 (COL10A1) expression and prognostic significance in gastric cancer based on bioinformatics

Abstract: Collagen type X alpha 1 (COL10A1) is a member of the collagen family and the main matrix component. However, COL10A1 expression and prognosis relationship remains unclear in gastric cancer (GC). Th...

Bioengineered Biochar As Smart Candidate For Resource Recovery Toward Circular Bio-Economy: A Review.

Abstract: Biochar's ability to mediate and facilitate microbial contamination degradation, as well as its carbon-sequestration potential, has sparked interest in recent years. The scope, possible advantages (economic and environmental), and future views are all evaluated in this review. We go over the many designed processes that are taking place and show why it is critical to look into biochar production for resource recovery and the role of bioengineered biochar in waste recycling. We concentrate on current breakthroughs in the fields of engineered biochar application techniques to systematically and sustainable technology. As a result, this paper describes the use of biomass for biochar production using various methods, as well as its use as an effective inclusion material to increase performance. The impact of biochar amendments on microbial colonisation, direct interspecies electron transfer, organic load minimization, and buffering maintenance is explored in detail. The majority of organic and inorganic (heavy metals) contaminants in the environment today are caused by human activities, such as mining and the use of chemical fertilizers and pesticides, which can be treated sustainably by using engineered biochar to promote the establishment of a sustainable engineered process by inducing the circular bioeconomy.

MicroRNA miR-330-3p suppresses the progression of ovarian cancer by targeting RIPK4.

Abstract: Previous studies reported that miR-330-3p was involved in the progression of several cancers, but the potential roles of miR-330-3p in ovarian cancer (OC) were unclear. In the current study, we aimed to explore the expression pattern and functions of miR-330-3p in OC. The expression level of miR-330-3p in OC tissues and cell lines was detected using RT-qPCR. The proliferation, migration and invasion of OC cells were detected using CCK-8 assay and transwell assay, respectively. Bioinformatics analysis and luciferase reporter assay were used to analyze the targeted binding site of miR-330-3p and RIPK4. The results showed that miR-330-3p was significantly downregulated in OC tissues and cell lines. Overexpression of miR-330-3p inhibited the proliferation, migration and invasion of OC cells. Mechanistically, a dual-luciferase reported assay showed that RIPK4 is a target gene of miR-330-3p. Furthermore, rescue experiments revealed that miR-330-3p suppressed the proliferation, migration and invasion of OC cells by targeting RIPK4. In summary, our findings indicated that miR-330-3p suppressed the progression of OC by targeting RIPK4. Our results indicated that miR-330-3p/RIPK4 axis might act as a novel therapeutic target for OC treatment.

LINC00839/miR-144-3p/WTAP (WT1 Associated protein) axis is involved in regulating hepatocellular carcinoma progression.

Abstract: The present work aimed to explore LINC00839 expression level and its function in hepatocellular carcinoma (HCC), and identify the downstream molecular mechanisms. qRT-PCR (Real-Time Quantitative Reverse Transcription PCR) and western blot were employed to detect mRNA and protein levels. Functional investigations were performed by flow cytometric-based apoptosis assay, CCK8 (Cell Counting Kit-8) assay, clone formation assay, Transwell migration and invasion assay. Functional interactions between LINC00839 and miR-144-3p or miR-144-3p and WTAP were validated by dual luciferase reporter assay. siRNA (small interfering RNA) was used for LINC00839 silencing, and microRNA mimic or inhibitor were employed to modulate miR-144-3p activity. LINC00839 was upregulated in HCC cells and tissues. Silencing LINC00839 suppressed the proliferation, invasion, migration of HCC cells and induced apoptosis. Additionally, LINC00839 served as a sponge to negatively impact on miR-144-3p activity, which contributed to the high expression of WTAP (WT1 Associated Protein) and the malignant phenotype of HCC cells. Our study revealed an oncogenic role of LINC00839 in HCC, and identified miR-144-3p/WTAP axis as downstream effectors mediating the oncogenic function of LINC00839. LINC00839 might serve as a potential therapeutic target and prognostic marker for HCC.

Identification of important genes related to ferroptosis and hypoxia in acute myocardial infarction based on WGCNA.

Abstract: Acute myocardial infarction (AMI) tends to cause severe heart failure and the population suffering from AMI gradually become younger. This study aims to determine the key genes associated with AMI, ferroptosis and hypoxia that could serve as novel biomarkers or potential therapeutic targets for AMI. There were 522 up-regulated genes and 119 down-regulated genes in GSE4648. Based on the expression of ferroptosis-related genes (FRGs) and hypoxia-related genes, the ferroptosis Z-score and the hypoxia Z-score calculated by ssGSEA were significantly higher in the infarcted area of AMI mice than that in the control group, and there was a notable positive correlation between ferroptosis Z-score and hypoxia Z-score. 6 modules were obtained by Weighted Gene Co-Expression Network Analysis (WGCNA), and 2 key modules and 66 key genes were screened out. Genes in the key modules were found mainly related to ERK1 and ERK2 cascade, cellular response to interleukin-1, TNF signaling pathway, and MAPK signaling pathway through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis using the clusterProfiler package. Protein-protein interaction (PPI) network analysis was carried out on the key genes and 10 hub genes (Atf3, Ptgs2, Cxcl1, Socs3, Hspa1b, Selp, Cxcl2, Il1b, Myd88, and S100a8) were obtained using STRING and Cytohubba. The expression of 9 hub genes except Cxcl1 was consistent in GSE4648 and GSE775. The transcription factors (TFs)-hub genes interaction network was constructed and 48 TFs were obtained using TRRUST. Finally, it was verified through the animal experiment that these hub genes were up-regulated in AMI mice myocardial tissues. This study offers new ideas for the disease prevention, diagnosis and treatment of AMI.

Characteristics of immune cell infiltration and associated diagnostic biomarkers in ulcerative colitis: results from bioinformatics analysis

Abstract: Ulcerative colitis (UC) is a type of refractory and recurrent inflammatory disorder that occurs in colon and rectum. Immune cell infiltration plays a critical role in UC progression; therefore, this study aims to explore potential biomarkers for UC and to analyze characteristics of immune cell infiltration based on the bioinformatic analysis. In this study, 248 differentially expressed genes (DEGs) were screened, and the top 20 immune-related hub genes and pathways were assessed. Moreover, four candidate diagnostic biomarkers (DPP10, S100P, AMPD1, and ASS1) were identified and validated. Immune cell infiltration analysis identified 13 differentially infiltrated immune cells (IICs) in UC samples compared to normal samples, and the result showed that two IICs only expressed in UC samples. In addition, the present research found that DPP10 was negatively correlated with neutrophils, S100P exhibited a positive correlation with resting CD4 memory T cells, AMPD1 was positively correlated with M2 macrophages, and ASS1 was inversely associated with neutrophils and positively related to CD8 T cells. Taken together, these findings indicated that DPP10, S100P, AMPD1, and ASS1 may act as diagnostic biomarkers for UC, and that differential IICs may help to illustrate the progression of UC.

A Review of the Therapeutic and Biological Effects of Edible and Wild Mushrooms.

Abstract: Throughout history, mushrooms have occupied an inseparable part of the diet in many countries. Mushrooms are considered a rich source of phytonutrients such as polysaccharides, dietary fibers, and other micronutrients, in addition to various essential amino acids, which are building blocks of vital proteins. In general, mushrooms offer a wide range of health benefits with a large spectrum of pharmacological properties, including antidiabetic, antioxidative, antiviral, antibacterial, osteoprotective, nephroprotective, hepatoprotective, etc. Both wild edible and medicinal mushrooms possess strong therapeutic and biological activities, which are evident from their in vivo and in vitro assays. The multifunctional activities of the mushroom extracts and the targeted potential of each of the compounds in the extracts have a broad range of applications, especially in the healing and repair of various organs and cells in humans. Owing to the presence of the aforementioned properties and rich phytocomposition, mushrooms are being used in the production of nutraceuticals and pharmaceuticals. This review aims to provide a clear insight on the commercially cultivated, wild edible, and medicinal mushrooms with comprehensive information on their phytochemical constituents and properties as part of food and medicine for futuristic exploitation. Future outlook and prospective challenges associated with the cultivation and processing of these medicinal mushrooms as functional foods are also discussed.

Long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) sponges microRNA-124-3p to up-regulate phosphodiesterase 4B (PDE4B) to accelerate the progression of Parkinson's disease.

Abstract: Reportedly, long non-coding RNA (lncRNA) are crucial modulators in neurodegenerative diseases. Herein, we investigated the role of lncRNA nuclear enriched abundant transcript 1 (NEAT1) in Parkinson's disease (PD). In-vitro PD model was established based on SH-SY5Y cells treated with 1-methyl-4-phenylpyridinium (MPP+). NEAT1, microRNA (miR) -124-3p and phosphodiesterase 4B (PDE4B) expression levels were examined by qRT-PCR. CCK-8 assay and LDH release assay were adopted to delve into the cell viability and cytotoxicity, respectively. Besides, western blot was utilized to determine mTOR, p-mTOR and PDE4B expression levels. ELISA was executed to detect the levels of tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β) and interleukin 6 (IL-6). Dual-luciferase reporter assay and RIP assay were used to probe the relationship between miR-124-3p and NEAT1 or PDE4B. We demonstrated that, in SH-SY5Y cells treated with MPP+, NEAT1 and PDE4B expression levels were raised, while miR-124-3p expression was repressed; NEAT1 depletion or miR-124-3p overexpression increased the cell viability and suppressed cell injury. Besides, miR-124-3p was confirmed as the direct target of NEAT1, and its down-regulation counteracted the impact of NEAT1 depletion on SH-SY5Y cells. PDE4B was as the downstream target of miR-124-3p, and its overexpression weakens the impact of miR-124-3p on SH-SY5Y cells. Additionally, NEAT1 decoyed miR-124-3p to modulate PDE4B expression. Collectively, in MPP+-induced SH-SY5Y cells, NEAT1 depletion increases cell viability, represses cytotoxicity and reduces inflammatory response by regulating miR-124-3p and PDE4B expression levels, suggesting that NEAT1 may be a promising target for treating PD.

N6-methyladenosine (m6A)-mediated up-regulation of long noncoding RNA LINC01320 promotes the proliferation, migration, and invasion of gastric cancer via miR495-5p/RAB19 axis

Abstract: Gastric cancer is one of the most common malignant tumors. Long non-coding RNAs play crucial roles in gastric cancer progression. This study investigated the effect of LINC01320 on malignant behaviors of gastric cancer cells and explored its possible molecular mechanism. LINC01320 expression in gastric cancer tissues and cell lines was measured by qRT-PCR. Cell proliferation, transwell, and cell cloning assays were used to detect the effect of LINC01320 on the proliferation, migration, and invasion abilities, respectively, of gastric cancer cells. Bioinformatics analysis was used to predict the binding of miR-495-5p with LINC01320 and RAB19. A luciferase reporter assay was performed to verify their interactions. Finally, the N6-methyladenosine (m6A) modification of LINC01320 by METTL14 was identified through RIP experiments. LINC01320 was highly expressed in gastric cancer tissues and cells. LINC01320 overexpression promoted the proliferation, migration, and invasion of gastric cancer cells, while LINC01320 knockdown exerted the opposite effects. Moreover, miR-495-5p was predicted and demonstrated to target LINC01320 and RAB19. LINC01320 sponged miR-495-5p to regulate the expression of RAB19. Additionally, LINC01320-induced increases in cell viability, migration, and invasion of gastric cancer were alleviated by miR-495-5p and silenced RAB19. Furthermore, epigenetic studies showed that METTL14-mediated m6A modification led to LINC01320 up-regulation. METTL14 regulated the m6A modification of LINC01320. Overexpressed LINC01320 contributed to the aggressive phenotype of gastric cancer cells via regulating the miR-495-5p/RAB19 axis. This finding may provide new potential targets for treating gastric cancer.

Sustainable mitigation of heavy metals from effluents: Toxicity and fate with recent technological advancements.

Abstract: Increase in anthropogenic activities due to rapid industrialization had caused an elevation in heavy metal contamination of aquatic and terrestrial ecosystems. These pollutants have detrimental effects on human and environmental health. The majority of these pollutants are carcinogenic, neurotoxic, and are very poisonous even at very low concentrations. Contamination caused by heavy metals has become a global concern for which the traditional treatment approaches lack in providing a cost-effective and eco-friendly solution. Therefore, the use of microorganisms and plants to reduce the free available heavy metal present in the environment has become the most acceptable method by researchers. Also, in microbial- and phyto-remediation the redox reaction shifts the valence which makes these metals less toxic. In addition to this, the use of biochar as a remediation tool has provided a sustainable solution that needs further investigations toward its implementation on a larger scale. Enzymes secreted by microbes and whole microbial cell are considered an eco-efficient biocatalyst for mitigation of heavy metals from contaminated sites. To the best of our knowledge there is very less literature available covering remediation of heavy metals aspect along with the sensors used for detection of heavy metals. Systematic management should be implemented to overcome the technical and practical limitations in the use of these bioremediation techniques. The knowledge gaps have been identified in terms of its limitation and possible future directions have been discussed.

Recovery of resources from industrial wastewater employing electrochemical technologies: status, advancements and perspectives.

Abstract: In the last two decades, water use has increased at twice the rate of population growth. The freshwater resources are getting polluted by contaminants like heavy metals, pesticides, hydrocarbons, o ...

Long non-coding RNA LINC00649 regulates YES-associated protein 1 (YAP1)/Hippo pathway to accelerate gastric cancer (GC) progression via sequestering miR-16-5p.

Abstract: Although long non-coding RNA (LncRNA) LINC00649 is reported to be closely associated with acute myeloid leukemia (AML), prostate cancer and colorectal cancer, its role in regulating other types of cancer, such as gastric cancer (GC), has not been studied. This study analyzed the expression status of LINC00649 in GC tissues and cells by performing Real-Time qPCR analysis, and we found that LINC00649 tended to be enriched in cancerous tissues and cells but not in their normal counterparts, which were supported by the data from TCGA dataset. Next, by performing the gain- and loss-of-function experiments, we expectedly found that LINC00649 acted as an oncogene to accelerate GC cell proliferation, migration and epithelial-mesenchymal transition (EMT) in vitro and promote its tumorigenesis in vivo. Moreover, the online miRDB software predicted that miR-16-5p bound to both LINC00649 and 3' untranslated region (3'UTR) of YAP1 mRNA, which were validated by the following dual-luciferase reporter gene system assay and RNA pull-down assay. Finally, we proved that LINC00649 exerted its tumor-promoting effects in GC by regulating the miR-16-5p/YES-associated protein 1 (YAP1)/Hippo pathway. Mechanistically, knock-down of LINC00649 suppressed YAP1 expressions by releasing miR-16-5p, resulting in the recovery of the Hippo pathway, which suppressed the expression levels of the downstream oncogenes, including EGFR, SOX2 and OCT4, leading to the inhibition of the malignant phenotypes in GC cells. In conclusion, this study, for the first time, evidenced that LINC00649 promoted GC progression by targeting the miR-16-5p/YAP1/Hippo signaling pathway, which provided potential diagnostic and therapeutic indicators for GC treatment for clinical utilization.