Metformin affects transcriptomic pathways involved in cell survival, metabolism and angiogenesis in ovarian cancer cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA754426 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15446411.fastq.gz | Fastqsanger.gz | |||
| SRR15446413.fastq.gz | Fastqsanger.gz | |||
| SRR15446415.fastq.gz | Fastqsanger.gz | |||
| SRR15446417.fastq.gz | Fastqsanger.gz | |||
| SRR15446418.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 16 |
Similar Datasets
Project description:The objectives of the present study are to determine the effect of metformin on sphere formation, extracellular matrix invasion, and transcriptome profile of ovarian cancer (COVCAR) cells isolated from ascites of chickens that naturally developed ovarian cancer. Our results suggest that metformin treatment significantly decreased sphere formation and invasiveness of COVCAR cells. Pairwise statistical analysis of transcriptomic data using Deseq2 software revealed 0, 4, 365 genes that were differentially expressed (DEGs) in cells treated with 0.5, 1, 2 mM metformin-treated cells compared to controls, respectively.
2021-08-17 | GSE182084 | GEO
Project description:The biguanide metformin improves health and survival in male mice; however, it is unclear whether metformin will confer health and lifespan benefits to mice when started late in life. Two year-old mice fed on standard chow were treated with 1% metformin every-other week (EOW) or two consecutive weeks per month (2WM). EOW mice displayed improvements in healthspan reminiscent of mice on caloric restriction. The age-associated histopathological changes in liver and kidney were significantly reduced in EOW compared to 2WM or control mice. Some of the affected gene transcripts and metabolites were found to be risk predictors of metabolic disorder. Neither EOW nor 2WM mice exhibited extension in mean or maximum lifespan compared with control animals. Thus, metformin supplementation had a strong impact on reversing some of the deleterious effects of aging and resulted in an improvement of health in old male mice in the absence of an extension of lifespan.
2018-02-23 | GSE97074 | GEO
Project description:Metformin, a commonly used drug prescribed to treat type-2 diabetes, has been found to extend health span and delay cancer incidence and progression. Here, we report that starting chronic treatment with low dose of metformin (0.1% w/w in diet) at one year of age extends health and lifespan in male mice, while a higher dose (1% w/w) was toxic. Treatment with low dose metformin mimicked some of the benefits of calorie restriction, such as improved physical performance, increased insulin sensitivity, and reduced LDL and cholesterol levels. At a molecular level, metformin increased AMP-activated protein kinase activity without attenuation of the mitochondrial electron transport chain activities. Metformin treatment resulted in lower chronic inflammation and increased antioxidant protection, suggesting that the ability of metformin to improve health of laboratory animals may stem from these factors. Our results support that metformin supplementation could be beneficial in extending health and lifespan in humans.
2013-07-31 | GSE40936 | GEO
Project description:Metformin, a commonly used drug prescribed to treat type-2 diabetes, has been found to extend health span and delay cancer incidence and progression. Here, we report that starting chronic treatment with low dose of metformin (0.1% w/w in diet) at one year of age extends health and lifespan in male mice, while a higher dose (1% w/w) was toxic. Treatment with low dose metformin mimicked some of the benefits of calorie restriction, such as improved physical performance, increased insulin sensitivity, and reduced LDL and cholesterol levels. At a molecular level, metformin increased AMP-activated protein kinase activity without attenuation of the mitochondrial electron transport chain activities. Metformin treatment resulted in lower chronic inflammation and increased antioxidant protection, suggesting that the ability of metformin to improve health of laboratory animals may stem from these factors. Our results support that metformin supplementation could be beneficial in extending health and lifespan in humans. Groups of one-year old male B6C57/J mice were maintained on ad libitum AIN-93G SD diet, or a 40% caloric restriction of the AIN-93G SD diet, or an ad libitum AIN-93G diet supplemented with 0.1% w/w metformin for the rest of their lives. 5 mice from each of these 3 groups were selected and RNA was extracted from both muscle and liver tissue using 1.0mm glass beads in a Precellys 24 Tissue Homogenizer and Qiagen RNeasy Mini Kits for Fibrous Tissue according to manufacturer's specifications. Quality and quantity of the total RNA was checked with the Agilent 2100 bioanalyzer using RNA 6000 Nano chips. RNA samples were labeled using the Illumina TotalPrep RNA Amplification Kit. In short, 0.5g of total RNA was first converted into single-stranded cDNA with reverse transcriptase using an oligo-dT primer containing the T7 RNA polymerase promoter site and then copied to produce double-stranded cDNA molecules. The double stranded cDNA was cleaned and concentrated with the supplied columns and used in an overnight in-vitro transcription reaction where single-stranded RNA (cRNA) was generated and labeled by incorporation of biotin-16-UTP. Arrays were hybridized using a total of 0.75ug of biotin-labeled cRNA at 58 degrees C for 16 hours to Illumina's Sentrix MouseRef-8 v2 Expression BeadChips. Each BeadChip has ~24,000 well-annotated RefSeq transcripts with approximately 30-fold redundancy. The arrays were washed, blocked and the biotin labeled cRNA was detected by staining with streptavidin-Cy3. Arrays were scanned at a resolution of 0.8um using the Beadstation 500 X from Illumina and the data was extracted using the Illumina GenomeStudio software(v1.6.0). Any spots at or below the background were filtered out using an Illumina detection p value of 0.02 and above. The natural log of all remaining scores were used to find the avg and std of each array and the z-score normalization was calculated and presented below. Z-score = (raw value - avg)/std.
2013-07-31 | E-GEOD-40936 | biostudies-arrayexpress
Project description:Metformin improves cognition of aged mice by promoting cerebral angiogenesis and neurogenesis
| PRJNA590654 | ENA
Project description:We implemented transcriptomic analyses of hADSCs treated with metformin 6 days
2020-09-23 | GSE140714 | GEO
Project description:Metformin improves cognition of aged mice by promoting cerebral angiogenesis and neurogenesis [blood]
| PRJNA590664 | ENA
Project description:Metformin improves cognition of aged mice by promoting cerebral angiogenesis and neurogenesis [hADSCs]
| PRJNA590665 | ENA
Project description:Pancreatic cancer (pancreatic ductal adenocarcinoma: PDAC) is one of the most aggressive neoplastic diseases. Metformin use was associated with reduced pancreatic cancer incidence or better survival in diabetics. Metformin has been shown to inhibit PDAC cells survival and growth in vitro and in vivo. However, clinical trials using metformin failed to decrease pancreatic cancer progression in patients, raising important questions about molecular mechanisms that protect tumor cells from the antineoplastic activities of metformin. We confirm that metformin acts through inhibition of mitochondrial complex I, decreasing the NAD+/NADH ratio and that NAD+/NADH homeostasis determines metformin sensitivity in several cancer cell lines. Metabolites that can restore the NAD+/NADH ratio turned PDAC cells resistant to metformin. In addition, metformin treatment of PDAC cell lines induced a compensatory NAMPT expression increasing the pool of cellular NAD+. The NAMPT inhibitor FK866 sensitized PDAC cells to the antiproliferative effects of metformin in vitro and decreased cellular NAD+ pool. Intriguingly, FK866 combined with metformin increased survival in mice bearing KP4 cells xenografts but not in mice with PANC1 xenografts. Transcriptome analysis revealed that the drug combination reactivated genes in the p53 pathway and oxidative stress providing new insights about the mechanisms leading to cancer cell death.
2023-06-01 | GSE210562 | GEO
Project description:Metformin is a front-line drug in the treatment of type-2 diabetes mellitus (T2DM). In addition to its antigluconeogenic and insulin-sensitizing properties, it has emerged as a potent inhibitor of the inflammatory response of macrophages. Specifically, metformin has been shown to reduce transcript levels of Il1b, the gene encoding the pro-inflammatory cytokine interleukin (IL)-1b, during long-term exposure of macrophages to the bacterial cell-wall component lipopolysaccharide (LPS). However, the extent to which metformin affects the early transcriptional response to LPS has never been investigated. Here, we show that metformin affects transcript levels of a large yet selective subset of LPS-responsive genes after only two hours of LPS exposure, mostly counteracting the effect of LPS rather than enhancing it. The affected genes are implicated in a variety of biological functions, in particular cellular movement and trafficking. Intriguingly, metformin affects transcript levels of Il1b at this early time point as well, but through a molecular mechanism fundamentally different from the regulation observed after longer exposure. While down-regulation of Il1b by metformin during the late stages of the LPS response has been shown to rely on stabilization of hypoxia-inducible factor (HIF)-1α and production of IL-10, Il1b inhibition at the early stage requires AMP-activated protein kinase (AMPK) activation but is independent of HIF-1α and IL-10. These results reveal an unexpected complexity in the anti-inflammatory properties of metformin and demonstrate that Il1b is down-regulated by distinct mechanisms in the early and late stages of the LPS response.
2021-08-30 | GSE131348 | GEO