Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

HCT116 colorectal cancer cells treated with 2.5 mM Metformin

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE171478 | GEO | 2024/04/05

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

HCT116 colorectal cancer cells treated with 2.5 mM Metformin

Project description:HCT116 colorectal cancer cells treated with 2.5 mM Metformin

| PRJNA719792 | ENA

Colorectal cancer cell lines with SETDB1 depletion [RNA-seq]

Project description:We performed RNA sequencing analysis of three colorectal cancer cell lines (Caco2, HCT116, SW480) with SETDB1 knockdown. Samples were obtained after flow cytometry sorting according to KRT20 expression level.

2019-08-07 | GSE135460 | GEO

Metformin induces chromosome reorganization and changes in gene expression in normal human fibroblasts

Project description:We report the effects of metformin treatment on the transcriptome of normal human dermal fibroblasts isolated from foreskin (designated 2DD). We sequenced mRNA from 2 replicates of proliferative (PRO) and 2DD cells treated with two concentrations of metformin (0.5mM and 1.0 mM;5 days exposure). Comparative analyses with PRO transcripts a baseline indicate that fibroblsts exposed to different concentration of metformin result in differnetial transcript profiles.

2018-09-01 | GSE104458 | GEO

Effect of metformin on gene expression in mammary tissues in association with epithelial cell reprogramming in FVB/N mouse model

Project description:Metformin shows promise in breast cancer prevention, but its underlying mechanisms remain unclear. This study investigated the impact of metformin on the repopulation dynamics of mammary epithelial cells (MECs) and the signaling pathways in non-tumorigenic FVB/N mice. The mice were treated with metformin for 10 weeks, followed by morphogenesis, flow cytometry, analyses of MEC stemness, and RNA sequencing. The study findings indicated that metformin treatment in adult mice reduced mammary gland proliferation, as demonstrated by decreased Ki67+ cells and lateral bud formation. Additionally, metformin significantly reduced both basal and mammary repopulating unit subpopulations, indicating an impact on mammary epithelial cell repopulation. Mammosphere, colony-forming cell, and 3D culture assays revealed that metformin adversely affected mammary epithelial cell stemness. Furthermore, metformin downregulated signaling in key pathways including AMPK/mTOR, MAPK/Erk, PI3K/Akt, and ER, which contribute to its inhibitory effects on mammary proliferation and stemness. Transcriptome analysis with RNA sequencing indicated that metformin induced significant downregulation of genes involved in multiple critical pathways. KEGG-based pathway analysis indicated that genes in PI3K/Akt, focal adhesion, ECM-receptor, small cell lung cancer and immune-modulation pathways were among the top groups of differentially regulated genes. In summary, our research demonstrates that metformin inhibits MEC proliferation and stemness, accompanied by the downregulation of intrinsic signaling. These insights suggest that the regulatory effects of metformin on premalignant mammary tissues could potentially delay or prevent the onset of breast cancer, offering a promising avenue for developing new preventive strategies.

2024-08-02 | GSE269308 | GEO

Metformin affects transcriptomic pathways involved in cell survival, metabolism and angiogenesis in ovarian cancer cells

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

Metformin restrains ZIKV replication and alleviates virus-induced inflammatory responses in microglia

Project description:C20 were pre-treated with metformin at specified concentration (5 mM) for 2 h, followed by ZIKV infection at MOI 3. After infection of 1.5 h, cells were washed three times with PBS. Medium containing metformin was again supplemented and maintained during the culture. The total RNA of samples at 16 and 48 h were extracted for RNA-seq analysis. We then performed differential expression analysis using data obtained by RNA-seq of ZIKV infection and metformin treatment (16 h and 48 h).

2023-05-03 | GSE231200 | GEO

Gene expression analysis of MCF12A human breast cultures exposed to ethanol or acetaldehyde [4 weeks]

Project description:Alcoholism is associated with breast cancer incidence and progression, and moderate chronic consumption of ethanol is a risk factor. The mechanisms involved in alcohol's oncogenic effects are unknown, but it has been speculated that they may be mediated by acetaldehyde. Here, we use the immortalized normal human epithelial breast cell line MCF-12A to determine whether short- or long-term exposure to ethanol or to acetaldehyde, using in vivo compatible ethanol concentrations, induces their oncogenic transformation and/or the acquisition of epithelial mesenchymal transition (EMT). Cultures of MCF-12A cells were incubated with 25 mM ethanol or 2.5 mM acetaldehyde for 1 week, or with lower concentrations (1.0-2.5 mM for ethanol, 1.0 mM for acetaldehyde) for 4 weeks. In the 4 wk incubation, cells were also tested for anchorage independence, including isolation of soft agar selected cells (SASC) from the 2.5 mM ethanol incubations. Cells were analyzed by immuno-cytofluorescence, flow cytometry, western blotting, DNA microarrays, RT/PCR, and assays for miRs. We found that short-term exposure to ethanol, but not, in general, to acetaldehyde, was associated with transcriptional upregulation of the metallothionein family genes, alcohol metabolism genes, and genes suggesting the initiation of EMT, but without related phenotypic changes. Long-term exposure to the lower concentrations of ethanol or acetaldehyde induced frank EMT changes in the monolayer cultures and in SASC as demonstrated by changes in cellular phenotype and mRNA expression. This suggests that low concentrations of ethanol, with little or no mediation by acetaldehyde, induce EMT and some traits of oncogenic transformation such as anchorage independence in normal breast epithelial cells. MCF12A monolayer cultures were exposed to ethanol or acetaldehyde for either 1 week or 4 weeks. Total RNA samples were assayed for gene expression and for microRNA expression.

2017-02-10 | GSE76951 | GEO

Gene expression analysis of MCF12A human breast cultures exposed to ethanol or acetaldehyde [1 week]

2017-02-10 | GSE76950 | GEO

The Warburg effect alters histone acetylation in cancer cells by influencing the utilization of HDAC and HAT mechanisms.

Project description:Microarray transcriptome analysis of siMock and siACL HCT116 cells treated with 0, 0.5, 2.0, and 5.0 mM butyrate over three days.

2012-12-01 | GSE41113 | GEO

Paramecium tetraurelia strain:51

Project description:Paramecium flow cytometry-based nucleus purification

| PRJNA327166 | ENA