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Expression data of LoVo cells treated by 10mM metformin for eigher 8 or 24h

ABSTRACT: Metformin is effective for prevention or treatment of various tumors. There are a lot of studies on the underlying mechanisms of metformin as respect to its anti-tumor action. We used microarrays to detail the global programme of gene expression underlying the anti-tumor effects of metformin on LoVo cells. Human derived LoVo cells were treated with metformin (10mM) for 8 and 24h, and the control and treated cells were harvested for RNA extraction and hybridization on Affymetrix microarrays.The samples were grouped as Met8h, Met24h, Con8h, and Con24h, respectively.

ORGANISM(S): Homo sapiens

SUBMITTER: houkai li

PROVIDER: E-GEOD-67342 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data of LoVo cells treated by 10mM metformin for eigher 8 or 24h

Project description:Metformin is effective for prevention or treatment of various tumors. There are a lot of studies on the underlying mechanisms of metformin as respect to its anti-tumor action. We used microarrays to detail the global programme of gene expression underlying the anti-tumor effects of metformin on LoVo cells.

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Deep Phosphoproteomic Elucidation of Metformin-Signaling in Heterogenous Colorectal Cancer Cells

Project description:The biguanide drug metformin is a safe and widely prescribed drug for type 2 diabetes. Interestingly, hundreds of clinical trials were set to evaluate the potential role of metformin in the prevention and treatment of cancer including colorectal cancer (CRC). However, the metformin-induced cell signaling remains controversial. To interrogate cell signaling events and networks in CRC and explore the druggability of the metformin-rewired phosphorylation network, we performed a proteomic and phosphoproteomic analysis on a panel of 12 molecularly heterogeneous CRC cell lines. Using in-depth data-independent analysis mass spectrometry (DIA-MS), we profiled a total of 10,142 proteins and 56,080 phosphosites (P-sites) in CRC cells treated with metformin for 30 minutes and 24 hours. Our results indicate that metformin tends to not trigger or inhibit significant immediate phosphorylation events. Instead, it primarily remodels cell signaling in the long-term. Strikingly, the phosphorylation response to metformin was highly heterogeneous in the CRC panel. We further performed a network analysis to systematically estimate kinase/phosphatase activities and reconstruct signaling cascades in each cell line. We created a “MetScore” which catalogs the most consistently perturbed P-sites among CRC cells for future studies. Finally, we leveraged the metformin P-site signature to identify pharmacodynamic interactions, revealing and confirming a number of candidate metformin-interacting drugs, including navitoclax, a BCL-2/BCL-xL inhibitor. Together, we provide a state-of-the-art phosphoproteomic resource to explore the metformin-induced cell signaling for potential cancer therapeutics.

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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.

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Transcription profiling of the effect of metformin (50mg/kg,400mg/kg) on gene expression in livers of db/db mice

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