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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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE67342 | GEO | 2015/03/31

SECONDARY ACCESSION(S): PRJNA279831

REPOSITORIES: GEO

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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. 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.

2015-03-31 | E-GEOD-67342 | biostudies-arrayexpress

Metformin regulated genes in human prostate cancer cells

Project description:The biguanide metformin has been shown to not only reduce circulating glucose levels but also suppress in vitro and in vivo growth of prostate cancer. However, the mechanisms underlying the anti-tumor effects of metformin in advanced prostate cancers are not fully understood. The goal of the present study was to define the signaling pathways regulated by metformin in androgen-receptor (AR) positive, castration-resistant prostate cancers. Our group used RNA sequencing (RNA-seq) to examine genes regulated by metformin within the C4-2 human prostate cancer cell line. Western blot analysis and quantitative RT-PCR were used to confirm alterations in gene expression and further explore regulation of protein expression by metformin. Data from the RNA-seq analysis revealed that metformin alters the expression of genes products involved in metabolic pathways, the spliceosome, RNA transport, and protein processing within the endoplasmic reticulum. Gene products involved in ErbB, insulin, mTOR, TGF-, MAPK, and Wnt signaling pathways are also regulated by metformin. A subset of metformin-regulated gene products were genes known to be direct transcriptional targets of p53 or AR. Together, our results suggest metformin regulates multiple pathways linked to tumor growth and progression within advanced prostate cancer cells.

2022-02-10 | GSE196343 | GEO

microRNA array of LoVo cells and LoVo-Small Extracellular Vesicles

Project description:LoVo cells were cultured in sEV-depleted (160,000xg, 16h) complete medium and the supernatant were collected after 72h. sEVs were purified and centrifuged at 100,000xg for 2.5h using a Beckman SW41Ti rotor to know the miRNA in LoVo cells and LoVo-Small Extracellular Vesicles

2019-07-01 | GSE117866 | GEO

Expression data from Irinotecan resistant LoVo cells comapred to parental LoVo cells

Project description:Irinotecan, an analogue of camptothecin, is frequently used in combination with various anticancer drugs or as a single agent in treatment of colorectal cancer. But drug resistance of tumor is still a major obstacle to overcome for the success of cancer treatment. In this study, We established chronic irinotecan resistant cell line for new marker to increase the sensitivity to irinotecan and investigated gene expression profiles of the irinotecan-resistant colorectal cancer cell line. To create stable CRC cell line chronically resistant to Irinotecan, LoVo cell was exposed to an initial Irinotecan concentration of 0.1 M-NM-<mol/L in RPMI 1640 supplemented with 10% FBS. When the growth of the cultured cells reaches at 80% confluency, cells were passaged twice at same drug concentration to ensure adaptation and then concentration of Irinotecan was sequentially increased in the same manner to 8 M-NM-<mol/L and then we investigated the gene expressions between parental colorectal cancer cell line, LoVo and Irinotecan resistant LoVo cell lines

2014-07-18 | E-GEOD-59501 | biostudies-arrayexpress

Gene expression profiling in LoVo-P compared with LoVo-C cells

Project description:The differential expression of mRNA in LoVo-P cells compared with LoVo-C cells was successfully detected using the Arraystar Human LncRNA/mRNAArray V4.0, that used for the global profiling of 20730 human mRNA and 40173 long non-coding RNA (LncRNA) transcripts.

2017-09-20 | GSE103989 | GEO

Gene expression profiling of tumor-infiltrating CD45+CD8+ cells and CD45- tumor cells of tumor bearing mice treated with metformin or anti-PD-1 Ab or both

Project description:B16 Mouse melanoma cells (MO5) grow in syngeneic C57BL/6 mice. Anti-PD-1 Ab as an Immunecheck point inhibitor and/or metformin were administered on day 7 after tumor inoculation to mice. The tumor growth was decreased by either anti-PD-1 Ab or metformin treatment. Anti- tumor effect was more pronounced by the combination therapy of anti-PD-1 Ab and metformin. The mechanism underlying the superior effect of the combination therapy to mono-therapies were investigated by RNA sequencing of tumor infiltrating CD8+ cells (CD8TILs) and tumor cells. As a result, CD8TILs with the combination therapy was found to express IFNg and GzmB and to activate IRF1/8, STAT1/2, NFkB, TBX21. Moreover, tumor cells were found to activate IRF1/8, STAT1/2, NFkB, indicating that tumor cells sharply responded to IFNg produced from CD8TILs. The IFNg was also found to downregulate metabolism both glycolysis and oxidative phosphorylation (OxPhos) of tumor cells, while it upregulates metabolism of CD8T cells. Collectively, the metabolic competition between CD8TILs and tumor cells was found to shift to the advantage of CD8TILs over tumor cells, resulting in the strong inhibition of tumor growth by the combination therapy of anti-PD-1 Ab and metformin.

2022-07-01 | GSE134191 | GEO

Distinct perturbation of the translatome by the anti-diabetic drug metformin

Project description:Reduced cancer incidence has been reported among type II diabetics treated with metformin. Metformin exhibits anti-proliferative and anti-neoplastic effects associated with inhibition of mTORC1, but the mechanisms are poorly understood. We provide the first genome-wide analysis of translational targets of canonical mTOR inhibitors (rapamycin and PP242) and metformin, revealing that metformin controls gene expression at the level of mRNA translation to an extent comparable to that of canonical mTOR inhibitors. Importantly, metformin's anti-proliferative activity can be explained by selective translational suppression of mRNAs encoding cell cycle regulators via the mTORC1/4E-BP pathway. Thus, metformin selectively inhibits mRNA translation of encoded proteins that promote neoplastic proliferation, motivating further studies of this compound and related biguanides in cancer prevention and treatment. MCF7 cells were treated with rapamycin, metformin or PP242 at concentrations that inhibited proliferation to 50% of control. Both cytoplasmic and polysome-associated mRNA was extracted from treatments and a vehicle treated control and probed with microarrays.

2012-05-20 | E-GEOD-36847 | biostudies-arrayexpress

Expression data from human colorectal cancer cell line LoVo

Project description:PEAK1 overexpression vector and negative control vector were transiently transfected into LoVo cells, respectively, and named LoVo-PEAK1 and LoVo-control groups. LoVo cells of different groups were determined to investigate the different expressions of mRNA using a global gene microarray.

2018-01-10 | GSE108947 | GEO

Genome-wide CRISPR screen identifies synthetic lethality between DOCK1 inhibition and metformin in liver cancer

Project description:To explore how DOCK1 deficiency enhances the anti-tumor effects of metformin, we performed RNA-seq analysis in PLC cells expressing NTC or shDOCK1 in the presence or absence of metformin.

2021-12-31 | GSE181521 | GEO

A whole-genome CRISPRa screening metformin resistance related gene in prostate cancer

Project description:Metformin is a classic type II diabetes drug which has possessed anti-tumor properties for various cancers. However, different cancers do not respond to metformin with the same effectiveness or acquire resistance. Thus, searching for vulnerabilities of metformin-resistant prostate cancer is a promising strategy to improve the therapeutic efficiency. A genome-scale CRISPR-Cas9 activation library targeting 23430 genes is conducted to identify the genes that confer resistance to metformin in prostate cancer cells.

2020-10-14 | GSE159467 | GEO

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