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KLF5 promotes a mixed basal, club, and hillock epithelial cell identity in castration-resistant prostate cancer

ABSTRACT: KLF5 promotes a mixed basal, club, and hillock epithelial cell identity in castration-resistant prostate cancer

PROVIDER: PRJNA1108521 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28923860_1.fastq.gz	Fastqsanger.gz
	SRR28923860_2.fastq.gz	Fastqsanger.gz
	SRR28923861_1.fastq.gz	Fastqsanger.gz
	SRR28923861_2.fastq.gz	Fastqsanger.gz
	SRR28923862_1.fastq.gz	Fastqsanger.gz

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KLF5 promotes a mixed basal, club, and hillock epithelial cell identity in castration-resistant prostate cancer

Project description:Inhibiting the androgen receptor (AR) is effective for advanced prostate cancers because of their AR-dependent luminal epithelial cell identity. Tumors progress during therapy to castration resistant prostate cancer (CRPC) by restoring AR signaling and maintaining luminal identity or by converting through lineage plasticity to a neuroendocrine identity (NEPC) or double negative CRPC lacking luminal and neuroendocrine identity (DNPC). Here, we show that DNPC cells express genes defining basal, club, and hillock epithelial cells from benign prostate. We identified KLF5 as a regulator of DNPC growth and expression of genes defining this mixed basal, club, and hillock cell identity. KLF5-mediated upregulation of RARG exposed a DNPC growth sensitivity to retinoic acid receptor agonists, which down-regulated KLF5 and up-regulated AR. These findings offer new CRPC classifications based on prostate epithelial cell identities, and nominate KLF5 and RARG as therapeutic targets for CRPC displaying a mixed basal, club, and hillock identity.

2025-01-27 | GSE266853 | GEO

Expression data from surface airway epithelial basal cells, ciliated cells, and club cells.

Project description:To identify key genes that define surface airway epithelial (SAE) basal cells, we FACS isolated basal, ciliated, and club cell populations as previously reported (Zhao et al., 2014; PMID: 25043474) and performed microarray analysis on isolated mRNA. For fractionating SAE into basal, club, and ciliated populations, cells were stained with EpCAM-PECy7 (eBiosciences), GSIβ4-FITC (Sigma), SSEA1-Alexa Fluor® 647 (BioLegend), and CD24-PE (BD Pharmingen) for 30 minutes on ice as previously described (Zhao et al., 2014), prior to FACS. Basal cells were considered EpCAM+ and GSIβ4+. Secretory cells were considered EpCAM+ and SSEA1+. Ciliated cells were considered EpCAM+, GSIβ4- and CD24+. Primary SAE cells were harvested from C57BL/6 mice and sorted into basal, ciliated, and club cell populations for the purpose of identifying enrichment of transcripts specific to each cell type population.

2018-04-30 | GSE111557 | GEO

KLF5 co-immunoprecipitation mass spectrometry

Project description:Lineage plasticity is a hallmark of pancreatic ductal adenocarcinoma (PDAC) and contributes to tumor heterogeneity and therapeutic resistance. Here, we identify KLF5 as a dynamic master regulator of epithelial lineage identity in PDAC, with dichotomous roles in promoting either classical or basal-like transcriptional programs. Through unbiased proteomic and genetic screens, we uncover the AAA+ ATPases RUVBL1 and RUVBL2 as essential coactivators of KLF5 across both lineage states. We demonstrate that ATP hydrolysis by RUVBL1/2 is required for the stable interaction with an intrinsically disordered region of KLF5, enabling its recruitment to lineage-specific enhancers and driving transcriptional regulation of identity-defining genes. Notably, small-molecule inhibitors of RUVBL1/2 ATPase activity, which have anti-PDAC activity in vivo, suppress KLF5-dependent transcription. These findings define a previously unrecognized mechanism of ATP hydrolysis-dependent transcriptional coactivation by AAA+ ATPases and highlight a potential therapeutic strategy for modulating aberrant lineage programs in cancer. This project contains files relative to a Co-IP MS with KLF5-MBP as bait.

2025-08-21 | PXD066112 | Pride

Potent androgen receptor inhibition unleashes oncogenic action of the KLF5 stem cell transcription factor in castration-resistant prostate cancer [ChIP-seq]

Project description:Advanced prostate cancer (PC) can be treated with endocrine therapies that inhibit transcriptional activity of the androgen receptor (AR). However, PC will ultimately evolve under the selection pressure of these therapies and progress to a lethal phenotype termed castration-resistant PC (CRPC). Recent studies suggest that de-differentiation away from an AR-driven luminal cell identity may be a key, early step. However, early therapy-induced mechanisms of prostate cancer cell de-differentiation are poorly understood. Here we show that the stem cell transcription factor Kruppel-like factor 5 (KLF5) is transcriptionally repressed by AR, and de-repressed by enzalutamide. KLF5 expression is high in a subset of CRPC tissues, but low in primary adenocarcinoma. KLF5 functioned as oncogene in CPRC cells, promoting cellular migration, anchorage-independent growth, expression of basal cell markers, and transcriptional signatures of CRPC lineage plasticity, but had modest effects on cell proliferation. Chromatin immuno-precipitation (ChIP)-sequencing, RNA-sequencing, and co-immunoprecipitation experiments established a physical interaction between KLF5 and AR, and integrative analysis revealed that KLF5 and AR drive opposing transcriptional programs. We identified ERBB2 as a point of transcriptional convergence that was activated by KLF5 and repressed by AR. Accordingly, KLF5 expression levels in CRPC tissues correlated with predicted sensitivity to the dual EGFR inhibitor lapatanib, and the ERBB2-specific inhibitor mubritinib blocked KLF5-driven cell migration. Collectively, these findings implicate KLF5 as an AR-suppressed oncogene that drives early steps in CRPC de-differentiation and disease progression.

2021-09-21 | GSE148807 | GEO

Potent androgen receptor inhibition unleashes oncogenic action of the KLF5 stem cell transcription factor in castration-resistant prostate cancer [RNA-seq]

2021-09-21 | GSE148806 | GEO

KLF5 interacts with RUVBL1/2 to activate classical and basal lineage identities in PDAC [CRISPR]

Project description:We identify KLF5 as a lineage master regulator and a dependency in classical and basal subtypes of human PDAC. We integrate proteomic and genetic screens to reveal RUVBL1 and RUVBL2 as transcriptional coactivators of KLF5 in PDAC. We use biochemical and epigenomic methods to validate that KLF5-RUVBL1/2 complexes directly activate lineage identity genes in PDAC.

2025-10-08 | GSE295348 | GEO

KLF5 interacts with RUVBL1/2 to activate classical and basal lineage identities in PDAC [ChIP-seq]

2025-10-08 | GSE295354 | GEO

KLF5 interacts with RUVBL1/2 to activate classical and basal lineage identities in PDAC [RNA-seq]

2025-10-08 | GSE295349 | GEO

KLF5 interacts with RUVBL1/2 to activate classical and basal lineage identities in PDAC [SLAM-seq]

2025-10-08 | GSE295347 | GEO

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.

2019-10-01 | GSE124748 | GEO

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