Transcriptome Analysis of Liver cancer cell Huh-7 Treated with Metformin
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ABSTRACT:
PROVIDER: PRJNA785793 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17110790_1.fastq.gz | Fastqsanger.gz | |||
| SRR17110790_2.fastq.gz | Fastqsanger.gz | |||
| SRR17110791_1.fastq.gz | Fastqsanger.gz | |||
| SRR17110791_2.fastq.gz | Fastqsanger.gz | |||
| SRR17110792_1.fastq.gz | Fastqsanger.gz |
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Project description:Metformin is a kind of widely used antidiabetic agent, which regulates glucose homeostasis through inhibiting liver glucose production and increasing glucose uptake in muscle. Recent studies suggest that metformin exhibits anticancer properties in a variety of cancers. Although several antitumor mechanisms have been proposed for metformin action, its mode of action in human liver cancer remains not elucidated. In our study we investigated the underlying molecular mechanisms of metformin’s antitumor effect on Huh-7 cells of hepatocellular carcinoma (HCC) in vitro. RNA sequencing (RNA-seq) was performed to explore the effect of metformin on the transcriptome of Huh-7 cells. The results revealed that 4518 genes (with log2 fold change>1 or < -1, p-adjusted value<0.05) were differentially expressed in Huh-7 cells with treatment of 25mM metformin compared to 0mM metformin including 1812 up-regulated and 2706 down-regulated genes. Gene ontology and KEGG pathway analyses identified 54 classical pathways which were significantly enriched, and 16 pathways are closely associated with cancer, such as cell cycle, DNA replication, ECM-receptor interaction and so on. We selected 11 differentially expressed genes, which are closely associated with HCC to validate their differential expressions through quantitative real-time reverse transcription PCR (qRT-PCR). The result exhibited that the genes of FASN, MCM6, MCM5, MARCKS, FADS2, CXCL1, BMP4, SKP2, KNG1, PCNA were down-regulated and DUSP1 is significantly up-regulated in Huh-7 cells with treatment of 25mM metformin. These differentially expressed genes and pathways might play a crucial part in the antitumor effect of metformin, and might be potential targets of metformin treating HCC. Further investigations are required to evaluate the metformin mechanisms of anti-cancer action in vivo.
2021-12-05 | GSE190076 | GEO
Project description:Metformin is a kind of widely used antidiabetic drug that regulates glucose homeostasis by inhibiting liver glucose production and increasing muscle glucose uptake. Recently, some studies showed that metformin exhibits anticancer properties in a variety of cancers. Although several antitumor mechanisms have been proposed for metformin action, its mode of action in human liver cancer remains not elucidated. In our study, we investigated the underlying molecular mechanisms of metformin's antitumor effect on Huh-7 cells of hepatocellular carcinoma (HCC) in vitro. RNA sequencing was performed to explore the effect of metformin on the transcriptome of Huh-7 cells. The results revealed that 4,518 genes (with log2 fold change > 1 or < -1, adjusted p-value < 0.05) were differentially expressed in Huh-7 cells with treatment of 25-mM metformin compared with 0-mM metformin, including 1,812 upregulated and 2,706 downregulated genes. Gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses identified 54 classical pathways that were significantly enriched, and 16 pathways are closely associated with cancer, such as cell cycle, DNA replication, extracellular matrix-receptor interaction, and so on. We selected 11 differentially expressed genes, which are closely associated with HCC, to validate their differential expressions through a quantitative real-time reverse transcription-polymerase chain reaction. The result exhibited that the genes of fatty acid synthase, mini-chromosome maintenance complex components 6 and 5, myristoylated alanine-rich C-kinase substrate, fatty acid desaturase 2, C-X-C motif chemokine ligand 1, bone morphogenetic protein 4, S-phase kinase-associated protein 2, kininogen 1, and proliferating cell nuclear antigen were downregulated, and Dual-specificity phosphatase-1 is significantly upregulated in Huh-7 cells with treatment of 25-mM metformin. These differentially expressed genes and pathways might play a crucial part in the antitumor effect of metformin and might be potential targets of metformin treating HCC. Further investigations are required to evaluate the metformin mechanisms of anticancer action in vivo.
| S-EPMC8985428 | biostudies-literature
Project description:Optimal treatment for nonalcoholic steatohepatitis (NASH) has not yet been established, particularly for individuals without diabetes. We examined the effects of metformin, commonly used to treat patients with type 2 diabetes, on liver pathology in a non-diabetic NASH mouse model. Eight-week-old C57BL/6 mice were fed a methionine- and choline-deficient (MCD) + high fat (HF) diet with or without 0.1% metformin for 8 weeks.
2012-02-21 | E-GEOD-35961 | biostudies-arrayexpress
Project description:NOD-SCID mouse were treated with metformin for 11 and 24 days, the gene expression of tumors of mice treated with metformin were compared with respect to the expression of the tumors of mouse treated with vehicle (water). We evaluated the effect of Metformin (525mg/kg/day) for two times of treatment (11 days and 24 days) upon gene expression in tumors of mice treated or not with metformin. Metformin treatment decreased of tumor growth in both treatment regimens. A complete genomic analysis of transcriptomic status after treatment with metformin revealed an impact on the overall expression of transcripts.
2025-01-31 | GSE144395 | GEO
Project description:Metformin is a drug used in the treatment of type 2 diabetes mellitus. Various studies have elucidated its anticancer properties. In this study, the effect of metformin on the differentiation and tumor microenvironment of colorectal cancer cells (CRC) was evaluated. For our study, we have used HCT116 colorectal cancer cell line and treated the cells with Metformin. Maximum tolerable non-toxic dose of metformin on HCT116 cells was determined by MTT assay. Cells were treated with 2.5 mM Metformin for 2 weeks. Analysis of apoptosis was done by flow cytometry using Annexin V / PI. CSC population was determined by flow cytometry using CSC markers CD44 and CD166. Metformin's ability to induce differentiation in CSC was assessed by analyzing Cytokeratin 20 (CK20) by flow cytometry and CDX1 (transcription factor for CK20), by RT-QPCR. Expression of Ki67 (proliferation marker) was done by RT-QPCR. RNA was isolated from 2.5 mM Metformin-treated and untreated cells populations. Microarray of untreated and 2.5 mM Metformin-treated RNA was done to study the whole genome transcriptomic changes.
2024-04-05 | GSE171478 | GEO
Project description:Metformin is now the most widely prescribed oral anti-diabetic agent worldwide, taken by over 150 million people annually. Although metformin has been used clinically to treat type 2 diabetes for over 60 years. Its mechanism of action remains only partially understood and controversial. In particular, this includes whether AMPK plays a role in metformin suppression of liver glucose production. To address this issue, we knocked out the AMPK catalytic alpha1 and alpha 2 subunits in the liver of HFD-fed adult homozygous mice. These mice were treated with a physiological relevent metformin dose (50 mg/kg/day) for 3 weeks. Liver samples were collected.
2019-11-13 | GSE114234 | GEO
Project description:Rat liver and heart treated with either metformin or phenformin
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Project description:This experiment aimed to discover the effects of metformin on mouse liver and kidney tissue. The effects were seen by comparing the liver of the metformin group to the liver of a control group of mice treated given saline solution.
2018-08-02 | MSV000082688 | GNPS
Project description:Optimal treatment for nonalcoholic steatohepatitis (NASH) has not yet been established, particularly for individuals without diabetes. We examined the effects of metformin, commonly used to treat patients with type 2 diabetes, on liver pathology in a non-diabetic NASH mouse model.
2012-02-21 | GSE35961 | GEO
Project description:Background: Metformin, one of the first-line medication for the treatment of type 2 diabetes and gestational diabetes, has recently be suggested for targeting cardiovascular disease, cancer and aging. Therefore, current understanding of the mechanism of this drug is incompletely understood, and the function of multiple tissues, other than liver metabolism alone, may be influenced. Methods: The wildtype healthy mice treated with metformin were compared with controls (treated with double distilled water). The transcriptome changes with/without metformin treatment were probed by using high-throughput RNA-seq techniques Results: A comprehensive mouse transcriptome map with metformin treatment across ten tissues including aorta, eyeball, brain, adipose tissue, heart, kidney, liver, skeletal muscle, stomach and testis, was provided. Function enrichment, network characteristics and disease association of the differentially expressed genes were analyzed. We also compared our expression profiles with related microarray data in order to find conditions that share similar expression profiles with metformin treatment. Conclusions: This dataset could serve as a baseline resource for investigating the potential beneficial or adverse effects of metformin across different tissues.
2020-07-15 | GSE90755 | GEO