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To study the function of KLF5 in squamous cancers and gastrointestinal cancers [HiChIP]

ABSTRACT: To identify KLF5 target genes by integrating ChIP-seq, HiChIP and RNA-seq assays

ORGANISM(S): Homo sapiens

PROVIDER: GSE147854 | GEO | 2020/12/09

REPOSITORIES: GEO

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To study the function of KLF5 in squamous cancers and gastrointestinal cancers [RNA-seq]

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To study the function of KLF5 in squamous cancers and gastrointestinal cancers

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

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Inhibition of super enhancer downregulates the expression of KLF5 in basal-like breast cancers

Project description:The transcription factor KLF5 is highly expressed in basal-like breast cancer (BLBC). It promotes cell proliferation, survival, migration and stemness and serves as a potential therapeutic target. In this study, we first identified a super-enhancer (SE) located downstream of the KLF5 gene in BLBC. JQ-1, a BRD4-bromodomain inhibitor, inhibits the expression and activity of KLF5 in the HCC1806 and HCC1937 cell lines in time- and dose-dependent manners. A new BRD4 inhibitor, compound 870, is more potent than JQ-1 in terms of its ability to inhibit KLF5 and BLBC growth by inducing G1 phase cell cycle arrest. Additionally, a CDK7 inhibitor, THZ1, also inhibits KLF5 and BLBC growth. Our findings suggested that SE regulates KLF5 and that SE inhibitors could be an effective therapeutic strategy for treating BLBC.

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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.

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