Gene Expression Profiling of Estrogen Signaling in Colon Cancer Cell Line [CRC Project_addendum]
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PROVIDER: PRJNA448193 | ENA |
REPOSITORIES: ENA
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Project description:Gene Expression Profiling of Estrogen Signaling in Colon Cancer Cell Line [CRC Project]
| PRJNA448191 | ENA
Project description:We studied the transcriptional effect of estrogen in two colon cancer cell lines SW620 and SW480
2021-03-05 | GSE112565 | GEO
Project description:We studied the transcriptional effect of estrogen, G1, and ICI in two colon cancer cell lines SW620 and SW480
2021-03-05 | GSE112568 | GEO
Project description:Epidemiological studies highlight a strong association between obesity and colorectal cancer (CRC). This association appears stronger in men and a role for sex hormones is indicated by epidemiological studies. Especially estrogen is protective against CRC and correlated to several aspects of the metabolic syndrome. Anti-inflammatory and anti-tumorigenic effects of estrogen in colon have been demonstrated to act via estrogen receptor beta (ERβ). This led us to hypothesize that estrogenic signaling, through both systemic and local effects might modulate the colon microenvironment during HFD-induced obesity. In order to test our hypothesis mice were fed a control diet or a high fat diet (HFD) for 3 weeks and treated with different estrogenic ligands. In the present study, we demonstrate that there are sex-differences in the response to HFD-induced obesity and in the colon transcriptome. Both sexes develop obesity with an impaired circadian rhythm but the male metabolic profile is more sensitive to HFD and increased the colon epithelial cell proliferation. Females were resistant to impaired glucose metabolism, but HFD-feeding increased the infiltration of macrophages. Estrogen signaling in males, via ERα, presented anti-obesogenic effects. However, systemic and/or local activation of both ERα and ERβ restored the circadian rhythm in the males. In females, systemic activation of ERα restored the circadian rhythm, however, systemic and/or local activation of ERβ down-regulated the expression of macrophage markers. These results suggest that estrogen signaling through systemic and/or local activation of ERβ can regulate the colon microenvironment during HFD-induced obesity.
2020-10-07 | GSE149811 | GEO
Project description:Gene Expression Profiling of Estrogen Signaling in Colon Cancer Cell Line
| PRJNA448189 | ENA
Project description:Estrogen signaling modulates the colon microenvironment during obesity
| PRJNA630214 | ENA
Project description:Assess the full impact of estrogen receptor beta on transcription by a full transcriptome analysis of ERb-mediated gene regulation in the SW480 colon cancer cell line. The colon cancer cell line SW480 does not express endogenous ER but is made ERb-expressing by lentiviral transduction of an ERb expression cassette. Introduction of ERb makes it possible to study the role and function of ERb in colon cancer as well as the impact ERb has on its own (in the absence of ERa).
2011-02-18 | E-MEXP-1473 | biostudies-arrayexpress
Project description:Background. Most colorectal cancers (CRC) arise in a progression through adenoma to carcinoma phenotypes as a consequence of altered genetic information. Clinical progression of CRC may occur in parallel with distinctive signaling alterations. We designed multidirectional analyses integrating microarray-based data with biostatistics and bioinformatics to elucidate the signaling and metabolic alterations underlying CRC development in the adenoma-carcinoma sequence. Methodology/Principal Findings. Studies were performed on normal mucosa, adenoma, and CRC samples obtained during surgery or colonoscopy. Collections of cryostat sections prepared from the tissue samples were evaluated by a pathologist to control the relative cell type content. RNA was isolated from 105 macro- and 40 microdissected specimens. The measurements were done using Affymetrix GeneChip HG-U133plus2, and probe set data were generated using two normalization algorithms: MAS5 and GCRMA with LVS. The data were evaluated using pair-wise comparisons and data decomposition into SVD modes. The method selected for the functional analysis used the Kolmogorov-Smirnov test. Based on a consensus of the results obtained by two tissue handling procedures, two normalization algorithms, and two probe set sorting criteria, we identified six KEGG signaling and metabolic pathways (cell cycle, DNA replication, p53 signaling pathway, purine metabolism, pyrimidine metabolism, and RNA polymerase) that are significantly altered in both macro- and microdissected tumor samples compared to normal colon. On the other hand, pathways altered between benign and malignant tumors were identified only in the macrodissected tissues. Conclusion/Significance. Multidirectional analyses of microarray data allow the identification of essential signaling alterations underlying CRC development. Although the proposed strategy is computationally complex and labor–intensive, it may reduce the number of false results. Gene expression profiles of 40 tissue samples representing distant full-thickness normal colon, normal colon mucosa dissected from tumor, adenoma, and carcinoma. Gene expression profiles of 105 tissue samples representing colon carcinomas, adenocarcinomas, and normal colon samples.
2010-08-01 | E-GEOD-20916 | biostudies-arrayexpress
Project description:KSR1 signaling alters the translational landscape of human CRC cells to support their survival. To determine the effect of KSR1 on translatomes in colon cancer cells, we performed genome-wide polysome profiling. We stably expressed short hairpin RNA (shRNA) constructs targeting KSR1 or a non-targeting control in two K-Ras mutant CRC cell lines, HCT116 and HCT15. We isolated and quantified both total mRNA and efficiently translated mRNAs (associated with ≥ 3 ribosomes) using RNA sequencing. We used Anota2seq to calculate translation efficiency (TE) by comparing the differences in efficiently translated mRNAs to the total transcript of each mRNA.
2021-01-10 | GSE164492 | GEO
Project description:Inflammation is involved in both initiation and promotion of colorectal cancer (CRC), and patients with inflammatory bowel disease (IBC) have increased risk of developing CRC. Tumor necrosis factor alpha (TNFα) is a cytokine secreted by e.g. macrophages, and this signaling is deregulated in IBD and CRC. TNFα activates the pro-survival transcription factor complex NFκB, which is composed of several subunits including p65 (RELA). We recently characterized the genome-wide transcriptional impact by TNFα in two CRC cell lines, but how p65 binds the chromatin, its cistrome, in colorectal cancer cells has not been explored. We here used p65 chromatin immunoprecipitation followed by sequencing (ChIP-Seq) in HT29 and SW480 cells, and correlated with the transcriptomic impact of TNFα. Further, estrogen receptor beta (ERβ) has anti-inflammatory and anti-tumorigenic effects in colon cells and interacts with NFκB main targets. We have shown that ERβ impacts TNFα signaling in CRC cells and ERβ impacts the P65 cistrome.
2021-03-01 | GSE160856 | GEO