HCT116 colorectal cancer cells treated with 2.5 mM Metformin
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ABSTRACT:
PROVIDER: PRJNA719792 | ENA |
REPOSITORIES: ENA
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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:Differential gene expression analysis of C. glutamicum ATCC 13032 in presence of 2.5 mM indole compared to control conditions without indole. C. glutamicum ATCC 13032 cells were cultivated in CGXII minimal medium with 40 g per litre glucose in presence of 2.5 mM indole and harvested during exponential phase (o.d.600 4).
2020-12-31 | GSE159887 | GEO
Project description:Colorectal cancer (CRC) continues to be the third most common cancer globally, often diagnosed at advanced stages due to a lack of early biomarkers. Current therapeutic methods frequently exhibit variable efficacy, highlighting the need for new treatment strategies. Metformin, a widely used antihyperglycemic agent, has recently garnered attention for its potential anti-tumor properties. In this study, we evaluated the effects of tumor suppressor genes TP53 and CDKN1A (p21) on the efficacy of metformin in a KRAS-mutant CRC model, HCT116 cells (harboring a G13D mutation in KRAS). Using the parental (p53+/+, p21+/+) cells and isogenic knockout (KO) versions for p53 and p21, we assessed cell viability, cell cycle distribution, and their transcriptomic responses to metformin treatment. Metformin significantly reduced cell proliferation in a dose- and time-dependent manner, with parental cells exhibiting the greatest sensitivity (approximately 20% viability reduction at 2 mM and 40% reduction at 10 mM after 24 h, p<0.05; and a 40% viability reduction at 5 mM and 60-70% reduction at 10 mM after 48 h, p<0.01). The loss of p53 or p21 notably decreased this sensitivity, with p53 KO cells responding only after 48 h of treatment, and p21 KO cells responding only at the higher dose of 10 mM after an incubation time of 72 h. The cell cycle analysis indicated a substantial G0/G1 arrest in parental cells (from approximately 55% of untreated cells to around 65% with 8 mM metformin at 24 h, p<0.05), while p53-/- and p21-/- cells did not show significant arrest (p>0.05). Our transcriptomic profiling revealed extensive differential gene expression in parental cells (1399 DEGs; 902 downregulated, 497 upregulated), in contrast to the limited responses in p53-/- (270 DEGs) and p21-/- cells (32 DEGs). Importantly, key genes involved in DNA replication stress (FAM111A), MAPK signaling (DUSP5), and inflammation modulation (TNFAIP3) were commonly regulated across the genotypes. Our findings emphasize that metformin’s antiproliferative effects in KRAS-mutant CRC are significantly influenced by the p53–p21 tumor suppressor axis, offering a more defined rationale for genotype-based precision oncology strategies.
2025-09-30 | GSE300002 | GEO
Project description:Transcriptional response of Corynebacterium glutamicum ATCC 13032 to 2.5 mM indole
| PRJNA670725 | ENA
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.
2023-02-18 | PXD036826 | Pride
Project description:We report the single-cell RNA sequencing data obtained from MDA-MB-231 breast cancer cells cultured in standard DMEM (high glucose) media, or adapted to culture in standard DMEM (high glucose) media containing 2 mM metformin, and then cultured as mammospheres
2020-10-23 | GSE110949 | GEO
Project description:Transcriptional profiling of hPTTG1-/- HCT116 human colorectal cancer cells comparing hPTTG1-/- HCT116 cells transfected with pcDNA3.1, and with hPTTG1-/- HCT116 cells transfected with pcDNA3.1-hPTTG1 plasmid.
2014-01-02 | GSE26434 | GEO
Project description:Transcriptional profiling of hPTTG1-/- HCT116 human colorectal cancer cells comparing hPTTG1-/- HCT116 cells transfected with pcDNA3.1, and with hPTTG1-/- HCT116 cells transfected with pcDNA3.1-hPTTG1 plasmid. Two-condition experiment, pchyg vs. 7-2 and 18-2 cells. 1 control, 2 different transfected cells.
2014-01-02 | E-GEOD-26434 | biostudies-arrayexpress
Project description:Determination of the ion channel and transporters gene expression profile of Bevacizumab-adapted colorectal adenocarcinoma cells HCT116
2023-01-02 | GSE221948 | GEO
Project description:Transcriptional profiling of HCT116 cells transfected with either control siRNA or TET1 siRNA was analyzed using whole human genome microarrays. To identify genes regulated by TET1 in colorectal cancer, HCT116 cells were transfected with either control siRNA or TET1 siRNA, and total RNA was extracted from biologically duplicated samples.
2015-09-04 | E-GEOD-66512 | biostudies-arrayexpress