Showing papers in "Apoptosis in 2022"
TL;DR: This review focuses on the mechanisms of cell death, including apoptosis, mitotic catastrophe, senescence, autophagic cellDeath, pyroptosis, etc., following paclitaxel treatment, and the use of combinations to overcome drug resistance.
18 citations
TL;DR: In this paper , the most efficient and effective methods of detection of programmed cell death, along with their conventional and unconventional methods of detecting of have been critically reviewed systematically and categorized on the basis of morphological hallmarks and biomarkers to understand the principle, mechanism, application, advantages and disadvantages of each method.
Abstract: Programmed cell death is considered a key player in a variety of cellular processes that helps to regulate tissue growth, embryogenesis, cell turnover, immune response, and other biological processes. Among different types of cell death, apoptosis has been studied widely, especially in the field of cancer research to understand and analyse cellular mechanisms, and signaling pathways that control cell cycle arrest. Hallmarks of different types of cell death have been identified by following the patterns and events through microscopy. Identified biomarkers have also supported drug development to induce cell death in cancerous cells. There are various serological and microscopic techniques with advantages and limitations, that are available and are being utilized to detect and study the mechanism of cell death. The complexity of the mechanism and difficulties in distinguishing among different types of programmed cell death make it challenging to carry out the interventions and delay its progression. In this review, mechanisms of different forms of programmed cell death along with their conventional and unconventional methods of detection of have been critically reviewed systematically and categorized on the basis of morphological hallmarks and biomarkers to understand the principle, mechanism, application, advantages and disadvantages of each method. Furthermore, a very comprehensive comparative analysis has been drawn to highlight the most efficient and effective methods of detection of programmed cell death, helping researchers to make a reliable and prudent selection among the available methods of cell death assay. Conclusively, how programmed cell death detection methods can be improved and can provide information about distinctive stages of cell death detection have been discussed.
16 citations
TL;DR: In this paper , the authors discuss the role of BCL-2 proteins in normal development and organismal function and how defects in the control of apoptosis promote the development and therapy resistance of cancer.
Abstract: Acquired resistance to cell death is a hallmark of cancer. The BCL-2 protein family members play important roles in controlling apoptotic cell death. Abnormal over-expression of pro-survival BCL-2 family members or abnormal reduction of pro-apoptotic BCL-2 family proteins, both resulting in the inhibition of apoptosis, are frequently detected in diverse malignancies. The critical role of the pro-survival and pro-apoptotic BCL-2 family proteins in the regulation of apoptosis makes them attractive targets for the development of agents for the treatment of cancer. This review describes the roles of the various pro-survival and pro-apoptotic members of the BCL-2 protein family in normal development and organismal function and how defects in the control of apoptosis promote the development and therapy resistance of cancer. Finally, we discuss the development of inhibitors of pro-survival BCL-2 proteins, termed BH3-mimetic drugs, as novel agents for cancer therapy.
14 citations
TL;DR: Nobiletin (NOB) is a herbal-derived agent with fascinating anti-cancer properties that may induce cancer cell killing by modulating other mechanisms that are involved in programmed cell death mechanisms.
13 citations
TL;DR: Experimental research indicates that XIAP as a key molecule of cell death not only suppress caspases and apoptosis, but also regulates inflammatory signaling, mitogenic kinase signaling, cell proliferation as well as cell invasion and metastasis.
13 citations
TL;DR: In this article , the role and mechanism of LINC00511 in the progression of cervical cancer (CC) was investigated using real-time polymerase chain reaction (qRT-PCR) and dual-luciferase reporter gene experiments.
Abstract: Abstract Background Long non-coding RNA (lncRNA) exhibits a crucial role in multiple human malignancies. The expression of lncRNA LINC00511, reportedly, is aberrantly up-regulated in several types of tumors. Our research was aimed at deciphering the role and mechanism of LINC00511 in the progression of cervical cancer (CC). Method Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to quantify the expression levels of LINC00511, miR-497-5p and MAPK1 mRNA in CC tissues and cell lines. Cell counting kit-8 (CCK-8), 5-bromo-2’-deoxyuridine (BrdU) and Transwell assays were conducted for detecting the proliferation, migration and invasion of CC cells. Dual-luciferase reporter gene experiments were performed to verify the targeting relationships amongst LINC00511, miR-497-5p and MAPK1. Besides, MAPK1 expression in CC cells was detected via Western blot after LINC00511 and miR-497-5p were selectively regulated. Results Up-regulation of LINC00511 expression in CC tissues and cell lines was observed, which was in association with tumor size, clinical stage and lymph node metastasis of the patients. LINC00511 overexpression facilitated the proliferation, migration and invasion of CC cells, while opposite effects were observed after knockdown of LINC00511. Mechanistically, LINC00511 was capable of targeting miR-497-5p and up-regulating MAPK1 expression. Conclusion LINC00511/miR-497-5p/MAPK1 axis regulates CC progression.
10 citations
TL;DR: The present review paper summarizes the molecular mechanisms of pyroptotic signaling pathways and their pathophysiological impacts on the progress of acute pancreatitis and briefly presents some experimental compounds targeting pyroPTosis-regulated cell death for exploring novel therapeutic directions for the treatment and management of AP.
10 citations
TL;DR: In this paper , a benzofuran pyran hybrid compound 4e has been identified as a compound with osteogenic potential for glucocorticoid induced osteoporosis in male mice.
Abstract: Glucocorticoid induced osteoporosis (GIOP) is the second most leading cause of osteoporosis. We have identified a compound, a benzofuran pyran hybrid compound 4e that has osteogenic potential and we wanted to assess its efficacy in GIOP in male mice. We assessed the effect of dexamethasone and compound 4e on primary osteoblasts using various cell based and immunofluorescence assays. For in vivo studies we administered methylprednisolone and compound 4e as a prophylactic measure in male Balb/c mice for 28 days and then evaluated the effect on bone microarchitecture by microCT, bone formation by histology along with clinically relevant bone markers. Compound 4e preserved osteoblast differentiation as evident by higher ALP positive cells and mineralization in compound treated groups. Compound 4e also increased the expression of osteogenic genes. This compound guarded β-catenin expression both in vitro and in vivo as confirmed by western blot and immunofluorescence assays. This led to the preservation of bone microarchitecture and cortical thickness at 2.5 mg kg-1 and 5 mg kg-1 doses. Further compound 4e enhanced bone formation rate and regulated osteocyte death. The osteogenic potential of compound 4e was reflected by an increased level of serum marker osteocalcin and decreased levels of SOST and CTX-I. Overall, Compound 4e is able to overcome the catabolic effect of dexamethasone on bone by targeting the canonical WNT/β-catenin signaling as evidenced by both in vitro and in vivo studies.
10 citations
TL;DR: It is demonstrated that doxorubicin-mediated DNA damage induces STING mediated NF-κB activation in triple-negative as compared to ER/PR positive breast cancer cells and STING and IL-6 levels show a positive correlation in breast cancer patients and poor survival outcomes.
10 citations
TL;DR: In this paper , the authors used histological techniques to analyze glial and neuronal cells, and illuminated a massive degeneration of neuronal cells and changes in glial cells morphology in hippocampal samples.
Abstract: Recent investigations of COVID-19 have largely focused on the effects of this novel virus on the vital organs in order to efficiently assist individuals who have recovered from the disease. In the present study we used hippocampal tissue samples extracted from people who died after COVID-19. Utilizing histological techniques to analyze glial and neuronal cells we illuminated a massive degeneration of neuronal cells and changes in glial cells morphology in hippocampal samples. The results showed that in hippocampus of the studied brains there were morphological changes in pyramidal cells, an increase in apoptosis, a drop in neurogenesis, and change in spatial distribution of neurons in the pyramidal and granular layer. It was also demonstrated that COVID-19 alter the morphological characteristics and distribution of astrocyte and microglia cells. While the exact mechanism(s) by which the virus causes neuronal loss and morphology in the central nervous system (CNS) remains to be determined, it is necessary to monitor the effect of SARS-CoV-2 infection on CNS compartments like the hippocampus in future investigations. As a result of what happened in the hippocampus secondary to COVID-19, memory impairment may be a long-term neurological complication which can be a predisposing factor for neurodegenerative disorders through neuroinflammation and oxidative stress mechanisms.
10 citations
TL;DR: The suppression of miR-130b-3p may become an effective therapeutic strategy for IVDD because it can upregulate the autophagic flux and alleviate the IVDD via targeting ATG14 and PRKAA1.
TL;DR: The complex effects of pyroptosis on cancer development generally include inhibition of cancer cell viability, impacts on the invasion and migration of cancer cells, improvement of antitumor immunity, and enhancement of chemotherapy sensitivity are reviewed.
TL;DR: A novel pathway, Ambra1-Akt-FoxO1-Bim, is proposed, which regulates apoptosis and chemosensitivity in breast cancer cells, and may represent a potential target for breast cancer treatment.
TL;DR: It is found that p53 n6-methyladenosine (m6A) played a decisive role in regulating HCC sensitivity to chemotherapy via the p53 activator RG7112 and the vascular endothelial growth factor receptor inhibitor apatinib and it is hypothesized that a METTL3- m6A-p53 axis could be a potential target in HCC therapy.
TL;DR: HPV-negative cervical cancers are more likely diagnosed at non-squamous type, older ages, more advanced stage and metastases, and associated with poorer prognosis as compared to HPV-positive cervical cancer.
TL;DR: It is concluded that targeting OIP5-AS1 might be a promising cancer therapy approach because of its multiple functions in cancer, including in proliferation, apoptosis, autophagy, ferroptosis, cell cycle, migration, metastasis, invasion and cancer stem cells and drug resistance.
TL;DR: In this paper , a benzofuran pyran hybrid compound 4e has been identified as a compound with osteogenic potential for glucocorticoid induced osteoporosis in male mice.
Abstract: Glucocorticoid induced osteoporosis (GIOP) is the second most leading cause of osteoporosis. We have identified a compound, a benzofuran pyran hybrid compound 4e that has osteogenic potential and we wanted to assess its efficacy in GIOP in male mice. We assessed the effect of dexamethasone and compound 4e on primary osteoblasts using various cell based and immunofluorescence assays. For in vivo studies we administered methylprednisolone and compound 4e as a prophylactic measure in male Balb/c mice for 28 days and then evaluated the effect on bone microarchitecture by microCT, bone formation by histology along with clinically relevant bone markers. Compound 4e preserved osteoblast differentiation as evident by higher ALP positive cells and mineralization in compound treated groups. Compound 4e also increased the expression of osteogenic genes. This compound guarded β-catenin expression both in vitro and in vivo as confirmed by western blot and immunofluorescence assays. This led to the preservation of bone microarchitecture and cortical thickness at 2.5 mg kg-1 and 5 mg kg-1 doses. Further compound 4e enhanced bone formation rate and regulated osteocyte death. The osteogenic potential of compound 4e was reflected by an increased level of serum marker osteocalcin and decreased levels of SOST and CTX-I. Overall, Compound 4e is able to overcome the catabolic effect of dexamethasone on bone by targeting the canonical WNT/β-catenin signaling as evidenced by both in vitro and in vivo studies.
TL;DR: It is found for the first time that tumor-derived exosomal PTEN degrades PTEN through ubiquitination to regulate the tumor immune microenvironment and promote NPC growth and metastasis.
TL;DR: This study successfully established a model of diabetic zebrafish larvae, and transcriptome analysis was completed, and the results suggested that 10.59% of differentially expressed genes related to the apoptosis pathway need to be considered.
TL;DR: This review comprehensively summarizes the homeostasis of gastric cancer cells, but the potential therapeutic interventions for the targeting of mitochondria for Gastric cancer therapy are also highlighted and discussed.
TL;DR: It is suggested that USP1 inhibitor (ML323) could be used as a viable anti-ESCC approach because of the cytotoxity of ML323.
TL;DR: In this paper , the authors showed that lncRNA ENSMUST_147219 promoted the development of ischemic acute kidney injury by regulating the miR-221-5p/IRF6 pathway.
Abstract: Abstract Although previous studies have revealed that long noncoding RNAs (lncRNAs) regulate the progression of ischemic acute kidney injury (AKI), the exact role and mechanism of lncRNA ENSMUST_147219 in ischemic AKI are not clear. In the present study, lncRNA ENSMUST_147219 was induced by ischemic injury in vitro and in vivo. Functionally, lncRNA ENSMUST_147219 mediated apoptosis in mouse proximal tubule‐derived cell line (BUMPT). Mechanistically, lncRNA ENSMUST_147219 sponged the microRNA (miR)-221-5p to upregulate the expression of interferon regulatory factor 6 (IRF6) to drive apoptosis. Finally, knockdown of lncRNA ENSMUST_147219 markedly attenuated the ischemic AKI by targeting the miR-221-5p/IRF6 axis. Collectively, our data demonstrated that lncRNA ENSMUST_147219 promoted the development of ischemic AKI by regulating the miR-221-5p/IRF6 pathway, which could be considered a new therapeutic target for ischemic AKI.
TL;DR: It is found that c-Myc protein levels negatively correlated with AZD5991 EC50s in AML cell lines and primary patient samples, and AZD6001 combined with inhibition of c- myc synergistically induced apoptosis in AMl cell lines, and cooperatively targeted leukemia progenitor cells.
TL;DR: It is found that cell death could be triggered in yeast cells heterologoulsy expressing Bax α with concentrations of acetic acid that are not lethal to wild type cells, closely resembling the natural Bax function in the cellular context.
TL;DR: SKI knockdown reduced NP cell apoptosis and ECM degradation by inhibiting the Wnt/β-catenin signaling pathway, ultimately protecting against IDD, suggesting SKI may be an effective target for IDD treatment.
TL;DR: The expression of the GSDMD gene increases significantly during LPS-induced pyroptosis in RAW264.7 murine macrophage cells, confirming that glycolysis plays crucial roles in the increasing effect of LPS.
TL;DR: Functional annotation supported increased tricarboxylic acid cycle activity and decreased hypoxia signaling corroborated by metabolomics and found cuproptosis was decreased in ccRCC compared with normal kidney.
TL;DR: It is demonstrated that ACh exerted cytoprotection against H/R-induced apoptosis, autophagy and mitochondrial impairment through the activation of both muscarinic and nicotinic receptors.