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Journal ArticleDOI

Pseudogene PLGLA exerts anti-tumor effects on hepatocellular carcinoma through modulating miR-324-3p/GLYATL1 axis.

TL;DR: In this paper, the role of Plasminogen like A (PLGLA) in hepatocellular carcinoma (HCC) was explored using The Cancer Genome Atlas (TCGA) datasets.
About: This article is published in Digestive and Liver Disease.The article was published on 2021-11-12 and is currently open access. It has received 5 citations till now. The article focuses on the topics: Competing endogenous RNA & Cancer research.
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Journal ArticleDOI
TL;DR: It is demonstrated that miR-324-3p suppressed ovarian cancer progression by targeting the WNK2/RAS pathway and provides theoretical evidence for the clinical application potential of miR+3p.
Abstract: ABSTRACT Ovarian cancer (OC) has the highest mortality rate among gynecological cancers, which progresses owing to dysregulated microRNAs (miRNAs) expression. Our study attempts to reveal the mechanism by which decreased miR-324-3p expression suppresses OC proliferation. Quantitative real-time PCR, western blotting, in situ hybridization, and immunohistochemistry were performed to estimate miR-324-3p and WNK2 expression levels in OC cells and tissues. Cell Counting Kit-8, colony formation, EdU, and transwell assays were performed to analyze the influence of miR-324-3p and WNK2 on the proliferation and invasion ability of OC cells. Subsequently, xenograft models were established to examine the effects of WNK2 on OC cell proliferation in vivo, and databases and luciferase reporter assays were used to test the relationship between miR-324-3p and WNK2 expression. Then, we showed that miR-324-3p expression is decreased in OC cells and tissues, indicating its inhibitory effect on OC cell proliferation. Quantitative real-time PCR and luciferase reporter assays demonstrated that miR-324-3p inhibited WNK2 expression by directly binding to its 3’ untranslated region. WNK2, an upregulated kinase, promotes the proliferation and invasion of OC cells by activating the RAS pathway. Moreover, WNK2 can partly reverse the inhibitory effects of miR-324-3p on OC cell proliferation. Hence, we demonstrate that miR-324-3p suppressed ovarian cancer progression by targeting the WNK2/RAS pathway. Our study provides theoretical evidence for the clinical application potential of miR-324-3p. Graphical Abstract

3 citations

Journal ArticleDOI
TL;DR: Napsin B Aspartic Peptidase, Pseudogene (NAPSB) was associated with CD4 + T cell infiltration in pancreatic ductal adenocarcinoma as discussed by the authors .
Abstract: Napsin B Aspartic Peptidase, Pseudogene (NAPSB) was associated with CD4 + T cell infiltration in pancreatic ductal adenocarcinoma. However, the biological role of NAPSB in hepatocellular carcinoma (HCC) remains to be determined.The expression of NAPSB in HCC as well as its clinicopathological association were analyzed using data from several public datasets. qRT-PCR was used to verify the relative expression of NAPSB in patients with HCC using the Zhongnan cohort. Kaplan-Meier analyses, and univariate and multivariate Cox regression were conducted to determine the prognosis value of NAPSB on patients with HCC. Then enrichment analyses were performed to identify the possible biological functions of NAPSB. Subsequently, the immunological characteristics of NAPSB in the HCC tumor microenvironment (TME) were demonstrated comprehensively. The role of NAPSB in predicting hot tumors and its impact on immunotherapy and chemotherapy responses was also analyzed by bioinformatics methods.NAPSB was downregulated in patients with HCC and high NAPSB expression showed an improved survival outcome. Enrichment analyses showed that NAPSB was related to immune activation. NAPSB was positively correlated with immunomodulators, tumor-infiltrating immune cells, T cell inflamed score and cancer-immunity cycle, and highly expressed in immuno-hot tumors. High expression of NAPSB was sensitive to immunotherapy and chemotherapy, possibly due to its association with pyroptosis, apoptosis and necrosis.NAPSB was correlated with an immuno-hot and inflamed TME, and tumor cell death. It can be utilized as a promising predictive marker for prognosis and therapy in HCC.

3 citations

Journal ArticleDOI
TL;DR: In this paper , the functional and prognostic value of chromatin regulators in renal carcinoma patients was investigated using univariate Cox regression analysis and LASSO regression analysis to construct a risk model for predicting the prognosis of renal cancer.
Abstract: Renal carcinoma is a common malignant tumor of the urinary system. Advanced renal carcinoma has a low 5-year survival rate and a poor prognosis. More and more studies have confirmed that chromatin regulators (CRs) can regulate the occurrence and development of cancer. This article investigates the functional and prognostic value of CRs in renal carcinoma patients.mRNA expression and clinical information were obtained from The Cancer Genome Atlas database. Univariate Cox regression analysis and LASSO regression analysis were used to select prognostic chromatin-regulated genes and use them to construct a risk model for predicting the prognosis of renal cancer. Differences in prognosis between high-risk and low-risk groups were compared using Kaplan-Meier analysis. In addition, we analyzed the relationship between chromatin regulators and tumor immune infiltration, and explored differences in drug sensitivity between risk groups.We constructed a model consisting of 11 CRs to predict the prognosis of renal cancer patients. We not only successfully validated its feasibility, but also found that the 11 CR-based model was an independent prognostic factor. Functional analysis showed that CRs were mainly enriched in cancer development-related signalling pathways. We also found through the TIMER database that CR-based models were also associated with immune cell infiltration and immune checkpoints. At the same time, the genomics of drug sensitivity in cancer database was used to analyze the commonly used drugs of renal clear cell carcinoma patients. It was found that patients in the low-risk group were sensitive to medicines such as axitinib, pazopanib, sorafenib, and gemcitabine. In contrast, those in the high-risk group may be sensitive to sunitinib.The chromatin regulator-related prognostic model we constructed can be used to assess the prognostic risk of patients with clear cell renal cell carcinoma. The results of this study can bring new ideas for targeted therapy of clear cell renal carcinoma, helping doctors to take corresponding measures in advance for patients with different risks.
Posted ContentDOI
29 Dec 2022
TL;DR: Wang et al. as mentioned in this paper used univariate Cox regression analysis and LASSO regression analysis to select prognostic chromatin-regulated genes and use them to construct a risk model for predicting the prognosis of renal cancer.
Abstract: Abstract Background: Renal carcinoma is a common malignant tumor of the urinary system. Advanced renal carcinoma has a low 5-year survival rate and a poor prognosis. More and more studies have confirmed that chromatin regulators(CRs) can regulate the occurrence and development of cancer. This article aims to investigate the functional and prognostic value of CRs in renal carcinoma patients. Methods: mRNA expression and clinical information were obtained from the TCGA(The Cancer Genome Atlas)database. Univariate Cox regression analysis and LASSO regression analysis were used to select prognostic chromatin-regulated genes and use them to construct a risk model for predicting the prognosis of renal cancer. Differences in prognosis between high-risk and low-risk groups were compared using Kaplan-Meier analysis. In addition, we analyzed the relationship between chromatin regulators and tumor immune infiltration, and explored differences in drug sensitivity between different risk groups. Results: We constructed a model consisting of 11 CRs to predict the prognosis of renal cancer patients, and not only successfully validated its feasibility, but we also found that the 11 CR-based model was an independent prognostic factor. Functional analysis showed that CRs were mainly enriched in cancer development-related signaling pathways. We also found through the TIMER database that CR-based models were also associated with immune cell infiltration and immune checkpoints.At the same time, the GDSC(The Genomics of Drug Sensitivity in Cancer database)database was used to analyze the commonly used drugs of KIRC(Renal clear cell carcinoma) patients. It was found that patients in the low-risk group were sensitive to drugs such as axitinib, pazopanib, sorafenib, and gemcitabine, while those in the high-risk group may be sensitive to sunitinib. Conclusion: The chromatin regulator-related prognostic model we constructed can be used to assess the prognostic risk of patients with clear cell renal cell carcinoma. The results of this study can bring new ideas for targeted therapy of clear cell renal carcinoma, helping doctors to take corresponding measures in advance for patients with different risks.
Posted ContentDOI
27 Sep 2022
TL;DR: Wang et al. as mentioned in this paper used univariate Cox regression analysis and LASSO regression analysis to select prognostic chromatin-regulated genes and use them to construct a risk model for predicting the prognosis of renal cancer.
Abstract: Abstract Background: Renal carcinoma is a common malignant tumor of the urinary system. Advanced renal carcinoma has a low 5-year survival rate and a poor prognosis. More and more studies have confirmed that chromatin regulators(CRs) can regulate the occurrence and development of cancer. This article aims to investigate the functional and prognostic value of CRs in renal carcinoma patients. Methods: mRNA expression and clinical information were obtained from the TCGA(The Cancer Genome Atlas)database. Univariate Cox regression analysis and LASSO regression analysis were used to select prognostic chromatin-regulated genes and use them to construct a risk model for predicting the prognosis of renal cancer. Differences in prognosis between high-risk and low-risk groups were compared using Kaplan-Meier analysis. In addition, we analyzed the relationship between chromatin regulators and tumor immune infiltration, and explored differences in drug sensitivity between different risk groups. Results: We constructed a model consisting of 11 CRs to predict the prognosis of renal cancer patients, and not only successfully validated its feasibility, but we also found that the 11 CR-based model was an independent prognostic factor. Functional analysis showed that CRs were mainly enriched in cancer development-related signaling pathways. We also found through the TIMER database that CR-based models were also associated with immune cell infiltration and immune checkpoints.At the same time, the GDSC(The Genomics of Drug Sensitivity in Cancer database)database was used to analyze the commonly used drugs of KIRC(Renal clear cell carcinoma) patients. It was found that patients in the low-risk group were sensitive to drugs such as axitinib, pazopanib, sorafenib, and gemcitabine, while those in the high-risk group may be sensitive to sunitinib. Conclusion: The chromatin regulator-related prognostic model we constructed can be used to assess the prognostic risk of patients with clear cell renal cell carcinoma. The results of this study can bring new ideas for targeted therapy of clear cell renal carcinoma, helping doctors to take corresponding measures in advance for patients with different risks.
References
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Journal ArticleDOI
TL;DR: The GLOBOCAN 2020 estimates of cancer incidence and mortality produced by the International Agency for Research on Cancer (IARC) as mentioned in this paper show that female breast cancer has surpassed lung cancer as the most commonly diagnosed cancer, with an estimated 2.3 million new cases (11.7%), followed by lung cancer, colorectal (11 4.4%), liver (8.3%), stomach (7.7%) and female breast (6.9%), and cervical cancer (5.6%) cancers.
Abstract: This article provides an update on the global cancer burden using the GLOBOCAN 2020 estimates of cancer incidence and mortality produced by the International Agency for Research on Cancer. Worldwide, an estimated 19.3 million new cancer cases (18.1 million excluding nonmelanoma skin cancer) and almost 10.0 million cancer deaths (9.9 million excluding nonmelanoma skin cancer) occurred in 2020. Female breast cancer has surpassed lung cancer as the most commonly diagnosed cancer, with an estimated 2.3 million new cases (11.7%), followed by lung (11.4%), colorectal (10.0 %), prostate (7.3%), and stomach (5.6%) cancers. Lung cancer remained the leading cause of cancer death, with an estimated 1.8 million deaths (18%), followed by colorectal (9.4%), liver (8.3%), stomach (7.7%), and female breast (6.9%) cancers. Overall incidence was from 2-fold to 3-fold higher in transitioned versus transitioning countries for both sexes, whereas mortality varied <2-fold for men and little for women. Death rates for female breast and cervical cancers, however, were considerably higher in transitioning versus transitioned countries (15.0 vs 12.8 per 100,000 and 12.4 vs 5.2 per 100,000, respectively). The global cancer burden is expected to be 28.4 million cases in 2040, a 47% rise from 2020, with a larger increase in transitioning (64% to 95%) versus transitioned (32% to 56%) countries due to demographic changes, although this may be further exacerbated by increasing risk factors associated with globalization and a growing economy. Efforts to build a sustainable infrastructure for the dissemination of cancer prevention measures and provision of cancer care in transitioning countries is critical for global cancer control.

35,190 citations

Journal ArticleDOI
25 Nov 2009-Cell
TL;DR: The mesenchymal state is associated with the capacity of cells to migrate to distant organs and maintain stemness, allowing their subsequent differentiation into multiple cell types during development and the initiation of metastasis.

8,642 citations

Journal ArticleDOI
TL;DR: The reprogramming of gene expression during EMT, as well as non-transcriptional changes, are initiated and controlled by signalling pathways that respond to extracellular cues, and the convergence of signalling pathways is essential for EMT.
Abstract: The transdifferentiation of epithelial cells into motile mesenchymal cells, a process known as epithelial-mesenchymal transition (EMT), is integral in development, wound healing and stem cell behaviour, and contributes pathologically to fibrosis and cancer progression. This switch in cell differentiation and behaviour is mediated by key transcription factors, including SNAIL, zinc-finger E-box-binding (ZEB) and basic helix-loop-helix transcription factors, the functions of which are finely regulated at the transcriptional, translational and post-translational levels. The reprogramming of gene expression during EMT, as well as non-transcriptional changes, are initiated and controlled by signalling pathways that respond to extracellular cues. Among these, transforming growth factor-β (TGFβ) family signalling has a predominant role; however, the convergence of signalling pathways is essential for EMT.

6,036 citations

Journal ArticleDOI
05 Aug 2011-Cell
TL;DR: It is proposed that this "competing endogenous RNA" (ceRNA) activity forms a large-scale regulatory network across the transcriptome, greatly expanding the functional genetic information in the human genome and playing important roles in pathological conditions, such as cancer.

5,334 citations

Journal ArticleDOI
16 Jan 2014-Nature
TL;DR: Understanding this novel RNA crosstalk will lead to significant insight into gene regulatory networks and have implications in human development and disease.
Abstract: Recent reports have described an intricate interplay among diverse RNA species, including protein-coding messenger RNAs and non-coding RNAs such as long non-coding RNAs, pseudogenes and circular RNAs. These RNA transcripts act as competing endogenous RNAs (ceRNAs) or natural microRNA sponges — they communicate with and co-regulate each other by competing for binding to shared microRNAs, a family of small non-coding RNAs that are important post-transcriptional regulators of gene expression. Understanding this novel RNA crosstalk will lead to significant insight into gene regulatory networks and have implications in human development and disease.

2,869 citations