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:Liver macrophages are crucial to maintain liver homeostasis. However, upon metastatic seeding, cancer cells co-opt these macrophages to act as tumor-associated macrophages (TAMs), facilitating tumor growth and invasiveness. MicroRNAs (miRNAs) are key regulators of TAM pro-tumoral functions, thus modulating their expression in liver macrophages may constitute a novel approach for liver metastasis immunotherapy. In this study, we identify a myeloid specific miRNA, miR-342-3p, and investigate its anti-tumoral function in liver macrophages in the context of colorectal cancer liver metastasis (CRLM). To this aim, we harnessed lentiviral vectors (LV) to infer and modulate miRNA activity in liver macrophages in vitro and in vivo. We found that miR-342-3p was highly active in macrophages in the healthy liver, but downregulated in proximity to CRLM. Rescuing miR-342-3p activity through enforced miRNA expression induced a pro-inflammatory phenotype in liver macrophages, which was associated to reduced CRLM growth. Transcriptomic analysis revealed Slc7a11, a cysteine-glutamate antiporter associated with TAM pro-tumoral functions, as a major miR-342-3p target. Overall, our findings highlight the potential of miR-342-3p in TAM reprogramming to enhance anti-tumoral immunity.
2025-03-11 | GSE274045 | GEO
Project description:Liver macrophages are crucial to maintain liver homeostasis. However, upon metastatic seeding, cancer cells co-opt these macrophages to act as tumor-associated macrophages (TAMs), facilitating tumor growth and invasiveness. MicroRNAs (miRNAs) are key regulators of TAM pro-tumoral functions, thus modulating their expression in liver macrophages may constitute a novel approach for liver metastasis immunotherapy. In this study, we identify a myeloid specific miRNA, miR-342-3p, and investigate its anti-tumoral function in liver macrophages in the context of colorectal cancer liver metastasis (CRLM). To this aim, we harnessed lentiviral vectors (LV) to infer and modulate miRNA activity in liver macrophages in vitro and in vivo. We found that miR-342-3p was highly active in macrophages in the healthy liver, but downregulated in proximity to CRLM. Rescuing miR-342-3p activity through enforced miRNA expression induced a pro-inflammatory phenotype in liver macrophages, which was associated to reduced CRLM growth. Transcriptomic analysis revealed Slc7a11, a cysteine-glutamate antiporter associated with TAM pro-tumoral functions, as a major miR-342-3p target. Overall, our findings highlight the potential of miR-342-3p in TAM reprogramming to enhance anti-tumoral immunity.
2025-03-11 | GSE274044 | GEO
Project description:Liver macrophages are crucial to maintain liver homeostasis. However, upon metastatic seeding, cancer cells co-opt these macrophages to act as tumor-associated macrophages (TAMs), facilitating tumor growth and invasiveness. MicroRNAs (miRNAs) are key regulators of TAM pro-tumoral functions, thus modulating their expression in liver macrophages may constitute a novel approach for liver metastasis immunotherapy. In this study, we identify a myeloid specific miRNA, miR-342-3p, and investigate its anti-tumoral function in liver macrophages in the context of colorectal cancer liver metastasis (CRLM). To this aim, we harnessed lentiviral vectors (LV) to infer and modulate miRNA activity in liver macrophages in vitro and in vivo. We found that miR-342-3p was highly active in macrophages in the healthy liver, but downregulated in proximity to CRLM. Rescuing miR-342-3p activity through enforced miRNA expression induced a pro-inflammatory phenotype in liver macrophages, which was associated to reduced CRLM growth. Transcriptomic analysis revealed Slc7a11, a cysteine-glutamate antiporter associated with TAM pro-tumoral functions, as a major miR-342-3p target. Overall, our findings highlight the potential of miR-342-3p in TAM reprogramming to enhance anti-tumoral immunity.
2025-03-11 | GSE274046 | GEO
Project description:Liver macrophages are crucial to maintain liver homeostasis. However, upon metastatic seeding, cancer cells co-opt these macrophages to act as tumor-associated macrophages (TAMs), facilitating tumor growth and invasiveness. MicroRNAs (miRNAs) are key regulators of TAM pro-tumoral functions, thus modulating their expression in liver macrophages may constitute a novel approach for liver metastasis immunotherapy. In this study, we identify a myeloid specific miRNA, miR-342-3p, and investigate its anti-tumoral function in liver macrophages in the context of colorectal cancer liver metastasis (CRLM). To this aim, we harnessed lentiviral vectors (LV) to infer and modulate miRNA activity in liver macrophages in vitro and in vivo. We found that miR-342-3p was highly active in macrophages in the healthy liver, but downregulated in proximity to CRLM. Rescuing miR-342-3p activity through enforced miRNA expression induced a pro-inflammatory phenotype in liver macrophages, which was associated to reduced CRLM growth. Transcriptomic analysis revealed Slc7a11, a cysteine-glutamate antiporter associated with TAM pro-tumoral functions, as a major miR-342-3p target. Overall, our findings highlight the potential of miR-342-3p in TAM reprogramming to enhance anti-tumoral immunity.
2025-03-11 | GSE274043 | 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