MicroRNA-342-3p is a regulator of hepatocellular carcinoma regression
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ABSTRACT:
PROVIDER: PRJNA641039 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Hepatocellular carcinoma (HCC) is a cancer with global impact and largely refractory to current treatments. Novel treatment options are therefore urgently needed. MicroRNAs play important regulatory roles in HCCs and are emerging as promising therapeutic options against HCC. We identified tumor suppressor miRNAs that may attenuate tumor development and contribute to HCC regression. We identified miR-342-3p as a promising tumor suppressor miRNA. To understand how miR-342-3p affects the global landscape of gene expression, we transfected Huh7 human hepatoma cells with either the scramble control, or a mimic for miR-342-3p and performed mRNA expression profiling.
2020-12-31 | GSE152950 | GEO
Project description:RAW264.7 mouse macrophages were transfected with negative control and miR-342-3p mimics and subjected to microarray analysis 18 hours after the transfection. We used microarray to obtain global mRNA expression data of negative control and miR-342-3p mimics-transfected RAW264.7 cells.
2016-04-29 | GSE71642 | GEO
Project description:Accumulating evidence indicates that altered miRNA expression is crucially involved in lung cancer development, but only little has been elucidated about how MYC, an archetypical oncogene, is regulated by miRNAs, especially through a mechanism involving the MYC cofactor(s). In this study, we aimed at identifying miRNAs involved in the regulation of MYC transcriptional activity in lung cancers. To this end, we have taken an integrative approach with combinatorial usage of miRNA and mRNA expression profile datasets of patientsâ tumor tissues as well as those of MYC-inducible cell lines in vitro. We report here that in addition to miRNAs previously reported to be directly regulating or regulated by MYC including let-7 and miR-17-92, our strategy allowed us to identify miR-342-3p as the one capable of indirectly regulating MYC activity through direct repression of a MYC-cooperating molecule, E2F1. Furthermore, the miR-342-3p module activity, which we defined as a gene set reflecting experimentally substantiated influence of miR-342-3p on mRNA expression, was found to be inversely correlated with MYC activity reflected in the MYC module activity in three independent datasets of lung adenocarcinoma patients obtained by the Directorâs Challenge Consortium of the United States (P=1.94x10-73), the National Cancer Center of Japan (P=9.05x10-34) and our own in this study (P=3.37x10-6). Our integrative approach thus appears to be useful to elucidate inter-regulatory relationships between miRNAs and a protein coding-gene of interest, even those present in tumor tissues in patients, which still remains a challenge to better understand the pathogenesis of this devastating disease. Microarray analysis using a SurePrint G3 Human GE 8 x 60K Microarray G4851A (Agilent) was conducted.
2016-01-06 | E-GEOD-66759 | biostudies-arrayexpress
Project description:Accumulating evidence indicates that altered miRNA expression is crucially involved in lung cancer development, but only little has been elucidated about how MYC, an archetypical oncogene, is regulated by miRNAs, especially through a mechanism involving the MYC cofactor(s). In this study, we aimed at identifying miRNAs involved in the regulation of MYC transcriptional activity in lung cancers. To this end, we have taken an integrative approach with combinatorial usage of miRNA and mRNA expression profile datasets of patientsâ?? tumor tissues as well as those of MYC-inducible cell lines in vitro. We report here that in addition to miRNAs previously reported to be directly regulating or regulated by MYC including let-7 and miR-17-92, our strategy allowed us to identify miR-342-3p as the one capable of indirectly regulating MYC activity through direct repression of a MYC-cooperating molecule, E2F1. Furthermore, the miR-342-3p module activity, which we defined as a gene set reflecting experimentally substantiated influence of miR-342-3p on mRNA expression, was found to be inversely correlated with MYC activity reflected in the MYC module activity in three independent datasets of lung adenocarcinoma patients obtained by the Directorâ??s Challenge Consortium of the United States (P=1.94x10-73), the National Cancer Center of Japan (P=9.05x10-34) and our own in this study (P=3.37x10-6). Our integrative approach thus appears to be useful to elucidate inter-regulatory relationships between miRNAs and a protein coding-gene of interest, even those present in tumor tissues in patients, which still remains a challenge to better understand the pathogenesis of this devastating disease. Microarray analysis using a SurePrint G3 Human GE 8 x 60K Microarray G4851A (Agilent) was conducted. Tai, MeiChee
2016-01-06 | E-GEOD-66758 | biostudies-arrayexpress
Project description:Accumulating evidence indicates that altered miRNA expression is crucially involved in lung cancer development, but only little has been elucidated about how MYC, an archetypical oncogene, is regulated by miRNAs, especially through a mechanism involving the MYC cofactor(s). In this study, we aimed at identifying miRNAs involved in the regulation of MYC transcriptional activity in lung cancers. To this end, we have taken an integrative approach with combinatorial usage of miRNA and mRNA expression profile datasets of patients’ tumor tissues as well as those of MYC-inducible cell lines in vitro. We report here that in addition to miRNAs previously reported to be directly regulating or regulated by MYC including let-7 and miR-17-92, our strategy allowed us to identify miR-342-3p as the one capable of indirectly regulating MYC activity through direct repression of a MYC-cooperating molecule, E2F1. Furthermore, the miR-342-3p module activity, which we defined as a gene set reflecting experimentally substantiated influence of miR-342-3p on mRNA expression, was found to be inversely correlated with MYC activity reflected in the MYC module activity in three independent datasets of lung adenocarcinoma patients obtained by the Director’s Challenge Consortium of the United States (P=1.94x10-73), the National Cancer Center of Japan (P=9.05x10-34) and our own in this study (P=3.37x10-6). Our integrative approach thus appears to be useful to elucidate inter-regulatory relationships between miRNAs and a protein coding-gene of interest, even those present in tumor tissues in patients, which still remains a challenge to better understand the pathogenesis of this devastating disease.
2016-01-06 | GSE66759 | GEO
Project description:Accumulating evidence indicates that altered miRNA expression is crucially involved in lung cancer development, but only little has been elucidated about how MYC, an archetypical oncogene, is regulated by miRNAs, especially through a mechanism involving the MYC cofactor(s). In this study, we aimed at identifying miRNAs involved in the regulation of MYC transcriptional activity in lung cancers. To this end, we have taken an integrative approach with combinatorial usage of miRNA and mRNA expression profile datasets of patients’ tumor tissues as well as those of MYC-inducible cell lines in vitro. We report here that in addition to miRNAs previously reported to be directly regulating or regulated by MYC including let-7 and miR-17-92, our strategy allowed us to identify miR-342-3p as the one capable of indirectly regulating MYC activity through direct repression of a MYC-cooperating molecule, E2F1. Furthermore, the miR-342-3p module activity, which we defined as a gene set reflecting experimentally substantiated influence of miR-342-3p on mRNA expression, was found to be inversely correlated with MYC activity reflected in the MYC module activity in three independent datasets of lung adenocarcinoma patients obtained by the Director’s Challenge Consortium of the United States (P=1.94x10-73), the National Cancer Center of Japan (P=9.05x10-34) and our own in this study (P=3.37x10-6). Our integrative approach thus appears to be useful to elucidate inter-regulatory relationships between miRNAs and a protein coding-gene of interest, even those present in tumor tissues in patients, which still remains a challenge to better understand the pathogenesis of this devastating disease. Microarray analysis using a SurePrint G3 Human GE 8 x 60K Microarray G4851A (Agilent) was conducted.
2016-01-06 | GSE66758 | GEO
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Project description:Hepatocellular carcinoma (HCC) is one of the most common causes of death worldwide and the fourth most prevalent type of cancer. Whereas curative treatments such as liver transplantation, ablation or surgery are optimal for early stages, only paliative treatments are given to intermediate and advanced stages of the disease. Despite the introduction of immune regulators as first-line treatments for advanced stages, Sorafenib is still the standard of care in the clinical practice. In cell lysates, anti-tumoral properties of Sorafenib were related to upregulation of miR-200c-3p (anti-tumoral miRNA) at 6 hours of treatment and downregulation of miR-222-5p and miR-512-3p (pro-tumoral miRNAs) at 24 hours. We have identified these miRNA biomarkers of Sorafenib treatment response in plasma of patients with advanced HCC treated with Sorafenib. In particular, miR-200c-3p has been related to increased survival benefit whereas miR-222-5p and miR-512-3p have been related to worse prognosis. Our study has sequenced HepG2 cells treated with Sorafenib and miR-200c-3p inhibitor, and transfected with miR-222-5p and miR-512-3p mimics to unravel the molecular pathways governing Sorafenib response
2022-04-28 | GSE201695 | GEO