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Silcening YWHAE gene expression suppresses the proliferation of colon cancer cells by inducing gene differentially expressed.

ABSTRACT: In this study,YWHAE expression was silenced by RNA interference in colon cancer cell lines, and investigate the correlation between YWHAE expression and colon cancer proliferation,and differential expressed genes were analized by gene assay and qPCR technologe.The proliferation and colony formation ability of colon cancer cells were significantly reduced after YWHAE knockdown. More 1200 known genes were found to be involved in the YWHAE functions related tumorigenesis by genechip analysis, these genes related to cell proliferation/apoptosis and cell cycle process. qRT-PCR results showed an expression pattern consistent with that of the genechip analysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE78094 | GEO | 2016/02/20

SECONDARY ACCESSION(S): PRJNA312593

REPOSITORIES: GEO

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Silcening YWHAE gene expression suppresses the proliferation of colon cancer cells by inducing gene differentially expressed.

Project description:In this study,YWHAE expression was silenced by RNA interference in colon cancer cell lines, and investigate the correlation between YWHAE expression and colon cancer proliferation,and differential expressed genes were analized by gene assay and qPCR technologe.The proliferation and colony formation ability of colon cancer cells were significantly reduced after YWHAE knockdown. More 1200 known genes were found to be involved in the YWHAE functions related tumorigenesis by genechip analysis, these genes related to cell proliferation/apoptosis and cell cycle process. qRT-PCR results showed an expression pattern consistent with that of the genechip analysis. Lentivirus-mediated RNA interference was used to knockdown YWHAE expression in colon cancer cell lines. And cell proliferation assays . GeneChip analysis were carried out for mRNA expression profiling, followed, the expressed levels of mRNA and protein were measured by Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot , respectively.

2016-02-20 | E-GEOD-78094 | biostudies-arrayexpress

Silcening RAC1 expression suppresses the proliferation of colon cancer cells by inducing gene differentially expressed.

2016-02-20 | GSE78093 | GEO

Silcening RAC1 expression suppresses the proliferation of colon cancer cells by inducing gene differentially expressed.

Project description:In this study,RAC1 expression was silenced by RNA interference in colon cancer cell lines, and investigate the correlation between RAC1 expression and colon cancer proliferation,and differential expressed genes were analized by gene assay and qPCR technologe.The proliferation and colony formation ability of colon cancer cells were significantly reduced after RAC1 knockdown. More 1200 known genes were found to be involved in the RAC1 functions related tumorigenesis by genechip analysis, these genes related to cell proliferation/apoptosis and cell cycle process. qRT-PCR results showed an expression pattern consistent with that of the genechip analysis. Lentivirus-mediated RNA interference was used to knockdown RAC1 expression in colon cancer cell lines. And cell proliferation assays . GeneChip analysis were carried out for mRNA expression profiling, followed, the expressed levels of mRNA and protein were measured by Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot, respectively.

2016-02-20 | E-GEOD-78093 | biostudies-arrayexpress

Homo sapiens

Project description:Silcening YWHAE gene expression suppresses the proliferation of colon cancer cells by inducing gene differentially expressed.

| PRJNA312593 | ENA

Depletion of histone methyltransferase KMT9 inhibits lung cancer cell proliferation by inducing non-apoptotic cell death

Project description:Background: Lung cancer is the leading cause of cancer related death worldwide. Over the past 15 years no major improvement of survival rates could be accomplished. The recently discovered histone methyltransferase KMT9 as epigenetic regulator of prostate tumor growth has now raised hopes of enabling new cancer therapies. In this study we aimed to identify the function of KMT9 in lung cancer which has remained elusive so far. Methods: We linked full transcriptome and proteome analyses of A549 lung adenocarcinoma cells using RNA-Seq and mass spectrometry with functional cell culture, real-time proliferation and flow cytometry assays. Results: KMT9 is expressed in lung cancer tissue and cell lineswith high levels of KMT9 correlating with poor patient survival. We identified 460 overlapping genes and proteins that are deregulated upon knock-down of KMT9alpha in A549 cells. These genes cluster with proliferation, cell cycle and cell death gene sets as well as with subcellular organelles in gene ontology analysis. Knock-down of KMT9alpha inhibits lung cancer cell proliferation and induces non-apoptotic cell death in A549 cells. Conclusions: The novel histone methyltransferase KMT9 is crucial for proliferation and survival of lung cancer cells harboring various mutations. Small molecule inhibitors targeting KMT9 therefore should be further examined as potential milestones in modern epigenetic lung cancer therapy.

2020-05-26 | PXD014145 | Pride

Sturgeon chondroitin sulfates inhibit the proliferation of colorectal cancer cells by inducing cell cycle arrest and apoptosis

Project description:Cell proliferation assay and flow cytometric analysis were used to examine the effects of SCS treatment on viability and apoptosis of colon cancer cell HT-29 cells and normal colonic epithelial cell NCM460 cells. Transcriptomic and proteomic studies were used to identify the main targets of SCS. SCS showed little effect on the gene expression profile of NCM460 cells whereas188 genes and 10 proteins were differentially regulated in HT-29 cells after SCS treatment. Enrichment analysis of those genes / proteins showed that majority of them are involved in DNA replication, cell cycle progression, and apoptosis.

2021-09-15 | GSE179862 | GEO

RNA-seq analysis of gene expression in scramble and GPR126 knockdown colon cancer cells (HT-29)

Project description:Purpose: Identify genes regulated by GPR126 in colon cancer cells by RNA-seq analysis Methods: Use shRNAs to knock down GPR126 in HT-29 cells, total RNAs from scramble group (NC) and GPR126 knockdown group (Sh1) were subjected to RNA-sequencing. Results: Around 700 transcriptomes were up-regulated in GPR126 knockdown HT-29 cells, and 14000 transcriptomes were down-regulated in GPR126 knockdown HT-29 cells.GPR126 mainly regualtes genes from DNA synthesis and cell cycle-related pathways. Conclusions: Our study firstly showed the function of GPR126 regulating colon cancer cell proliferation by targeting genes invovled in DNA synthesis and cell cycle-related pathways.

2017-11-09 | GSE106696 | GEO

Colon cancer profiling

Project description:Expression profile was obtained for GeneChip probe sets among colon cancer specimens with or without the methylation of MLH1 promoter. Keywords: other

2005-08-26 | GSE2138 | GEO

Homo sapiens

Project description:PRDM1 inhibits proliferation of human colon cancer organoids

| PRJNA395153 | ENA

Fra-1 is a key driver of colon cancer metastasis and a Fra-1 classifier predicts disease-free survival

Project description:Background and Aim: Fra-1 (Fos-related antigen-1) is a member of the AP1 (activator protein-1) family of transcription factors. We have recently shown that Fra-1 is necessary for breast cancer cells to metastasize in vivo, and that breast cancer outcome can be predicted by a classifier comprising genes that are expressed in a Fra-1-dependent fashion. Here, we show that Fra-1 plays an important role also in colon cancer progression. Methods: We compared proliferation rates of parental and Fra-1-depleted colon cancer cells in vitro under 2D, 3D, and attachment-free conditions and in vivo upon subcutaneous and intravenous injections into mice. We also compared RNA expression profiles of colon cancer cells with and without Fra-1 expression. Results: Fra-1 depletion impair colony outgrowth of human colon cancer cells in soft agar and in suspension, whereas it does not affect proliferation on 2D culture plates. Consistent with this, upon subcutaneous injection into mice, tumors formed by Fra-1-depleted colon cancer cells are only three times smaller than those produced by control cells. In contrast, when injected intravenously, Fra-1 depletion causes 200-fold reduction in tumor burden. Consistent with the more aggressive characteristics of Fra-1-proficient tumors, the prognosis of colon cancer patients can be predicted by a Fra-1 classifier generated by comparing RNA profiles of parental and Fra-1-depleted colon cancer cells. Conclusions: Our results demonstrate that Fra-1 is an important determinant of the metastatic potential of human colon cancer cells, and suggest that a Fra-1 classifier can be used as a prognostic predictor in colon cancer patients.

2016-05-26 | GSE69415 | GEO

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