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Different forms of KLF5 regulate distinct sets of genes in prostate cancer cells [RNA-seq]

ABSTRACT: Different forms of KLF5 regulate distinct sets of genes in prostate cancer cells [RNA-seq]

PROVIDER: PRJNA680028 | ENA |

REPOSITORIES: ENA

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Different forms of KLF5 regulate distinct sets of genes in prostate cancer cells

Project description:Different forms of KLF5 regulate distinct sets of genes in prostate cancer cells

| PRJNA680026 | ENA

Different forms of KLF5 transcriptionally regulate distinct sets of genes in prostate cancer cells [ChIP-Seq]

Project description:Different forms of KLF5 transcriptionally regulate distinct sets of genes in prostate cancer cells [ChIP-Seq]

| PRJNA680029 | ENA

Different forms of KLF5 regulate distinct sets of genes in prostate cancer cells [RNA-seq]

Project description:To identify which genes are regulated by KLF5 and its acetylation, we performed RNA-Seq and bioinformatics analyses in KLF5-null prostate cancer cells expressing KLF5, KLF5KR, and KLF5KQ.

2020-12-19 | GSE161950 | GEO

Different forms of KLF5 transcriptionally regulate distinct sets of genes in prostate cancer cells [ChIP-Seq]

Project description:To identify which genes are directly regulated by KLF5 and its acetylation, we performed ChIP-Seq and bioinformatics analyses in KLF5-null prostate cancer cells expressing KLF5, KLF5KR, and KLF5KQ.

2020-12-19 | GSE161949 | GEO

Different forms of KLF5 regulate distinct sets of genes in prostate cancer cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-12-18 | GSE161951 | GEO

Tissue microenvironment shapes distinct sets of machineries to regulate ILC2 properties

Project description:Tissue microenvironment shapes distinct sets of machineries to regulate ILC2 properties

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Tissue microenvironment shapes distinct sets of machineries to regulate ILC2 properties [ATAC-seq]

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Tissue microenvironment shapes distinct sets of machineries to regulate ILC2 properties [RNA-seq]

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ChIP-Seq experiments of KLF5, GATA4 and GATA6 in YCC3/AGS/KATOIII cell lines

Project description:Three transcription factors KLF5, GATA4 and GATA6 are recurrently amplified in multiple gastric cancer cohorts, representing one type of lineage-survival oncogenes in gastric cancer. ChIP-Seq analysis of these three factors in multiple cell lines revealed that significant number of genomic sites are co-occupied by KLF5 and GATA4 and/or GATA6. Integrative analysis of ChIP-Seq and gene expression identified several targets of the three transcription factors in both cell lines and primary tumors, including HNF4A. These results suggest that KLF5, GATA4 and GATA6 interact and co-operate to regulate HNF4A and other genes to promote tumorigenesis in gastric cancer. ChIP-Seq experiments of KLF5, GATA4 and GATA6 were performed in three gastric cancer cell lines YCC3, AGS and KATOIII

2014-09-05 | E-GEOD-51705 | biostudies-arrayexpress

Over-expression and knockdown of KLF5

Project description:Activation of the Ras/Erk pathway upregulates expression of the Kruppel-like Factor 5 (KLF5) transcription factor, and KLF5 is a downstream mediator of Ras oncogenic signaling. Specifically, in bladder and colon cancer cell lines KLF5 upregulates the Ras-pathway target gene cyclin D1, and facilitates entry into the S phase of the cell cycle. Ras mutations are common in lung cancer, but a role for KLF5 in lung tumorigenesis has not been defined. To this end, we manipulated KLF5 expression in four Ras-mutant human lung adenocarcinoma cell lines to find that KLF5 significantly modulates anchorage-independent growth, a mutant Ras phenotype. However, in a mouse model of human lung adenocarcinoma, K-RasG12D does not critically require Klf5 to mediate oncogenesis or induce cyclin D1 expression. Patients with lung tumors expressing high levels of KLF5 have significantly better prognosis than those with low or no KLF5 expression (opposite of mutant Ras prognosis). The latter may be explained by KLF5 transcriptional repression of the ATP-binding cassette, sub-family G (WHITE), member 2 (ABCG2), an anthracycline transporter. In agreement with this, KLF5 knockdown cells display significantly more Hoechst “side population” and resistance to doxorubicin. In summary, while KLF5 is not an obligate partner in Ras oncogenic signaling, KLF5 control of ABCG2 expression is significant to patient survival.

2010-06-23 | GSE16555 | GEO

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