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FOXA1 regulates splicing-related gene expression and alternative splicing in prostate cancer cells

ABSTRACT: FOXA1 regulates splicing-related gene expression and alternative splicing in prostate cancer cells

PROVIDER: PRJNA795040 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17462522_1.fastq.gz	Fastqsanger.gz
	SRR17462522_2.fastq.gz	Fastqsanger.gz
	SRR17462523_1.fastq.gz	Fastqsanger.gz
	SRR17462523_2.fastq.gz	Fastqsanger.gz
	SRR17462524_1.fastq.gz	Fastqsanger.gz

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FOXA1 regulates splicing-related gene expression and alternative splicing in prostate cancer cells

Project description:Dysregulation of alternative splicing in prostate cancer is linked to transcriptional programs activated by canonical oncogenic transcription factors. However, the relative contribution of these factors to alternative splicing regulation is yet to be defined. We investigated the role of FOXA1 by performing deep RNA-seq on siRNA-treated (i.e. siFOXA1) and control (i.e. NSI) samples from prostate cancer cell lines. Using this data, we performed canonical parametric differential expression analysis between NSI and siFOXA1 samples to determine the effect of FOXA1 depletion on splicing related gene expression. We also identified FOXA1-regulated differentially alternatively spliced exons between NSI and siFOXA1 samples.

2022-09-27 | GSE193127 | GEO

The landscape of alternative splicing in aggressive prostate cancers

Project description:We sought to define the landscape of alternative pre-mRNA splicing in prostate cancers and the relationship of exon choice to known genetic driver alterations. To do so, we compiled a meta-dataset comprised of RNA-Seq samples from publicly available sources representing a range of phenotypes from normal tissue to drug resistant metastases. We subjected these samples to exon-level analysis with purpose-built software. We then correlated transcriptional signatures of cancer driver pathways with these alternative splicing events and discovered that Myc signaling was correlated with incorporation of a set of cassette exons found in RNA binding proteins. We experimentally verified this finding in a human prostate cell transformation assay. Our results connect changes in alternative pre-mRNA splicing to oncogenic alterations common in prostate and many other cancers. We also establish a role for Myc in regulating RNA processing by controlling the incorporation of nonsense mediated decay-determinant exons in RNA binding proteins.

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The pioneer transcription factors Foxa1 and Foxa2 regulate alternative RNA splicing during positive selection in the thymus

Project description:Here we show that the pioneer transcription factors Foxa1 and Foxa2 are required to regulate RNA splicing during positive selection at the transition from CD4+CD8+ double positive (DP) to single positive (SP thymocyte). Conditional deletion of both Foxa1 and Foxa2 from DP thymocytes led to a partial arrest at the transition from DP to SP, with a reduction in the number of cells undergoing positive selection, and reduced the number and maturation of both CD4SP and CD8SP populations, with a reduction in peripheral naïve CD4+ T-cells. Foxa1 and Foxa2 were required for physiological levels of expression of several genes which encoding splicing factors (Mbnl1, Sf3b1, Hnrnpa1) in cells undergoing positive selection. Within the positively selecting CD69+DP cells, alternative RNA splicing was dysregulated leading to more than 859 significantly differentially expressed exons compared to control, with many genes important for T cell development and for RNA splicing showing differentially used exons.

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FOXA1 regulates alternative splicing in prostate cancer.

Project description:Dysregulation of alternative splicing in prostate cancer is linked to transcriptional programs activated by AR, ERG, FOXA1, and MYC. Here, we show that FOXA1 functions as the primary orchestrator of alternative splicing dysregulation across 500 primary and metastatic prostate cancer transcriptomes. We demonstrate that FOXA1 binds to the regulatory regions of splicing-related genes, including HNRNPK and SRSF1. By controlling trans-acting factor expression, FOXA1 exploits an "exon definition" mechanism calibrating alternative splicing toward dominant isoform production. This regulation especially impacts splicing factors themselves and leads to a reduction of nonsense-mediated decay (NMD)-targeted isoforms. Inclusion of the NMD-determinant FLNA exon 30 by FOXA1-controlled oncogene SRSF1 promotes cell growth in vitro and predicts disease recurrence. Overall, we report a role for FOXA1 in rewiring the alternative splicing landscape in prostate cancer through a cascade of events from chromatin access, to splicing factor regulation, and, finally, to alternative splicing of exons influencing patient survival.

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Effect of FOXA1 overexpression in prostate cancer

Project description:FOXA1 is a transcription factor which aids AR function in prostate. There is controversary over the effect of high FOXA1 level has on prostate cancer so we forced the overexpression in the LNCaP prostate cancer cell line. LNCaP prostate cancer cell line was transfected with GFP control plasmid or plasmid containing FOXA1 full length cDNA. The effect on gene expression was assessed by microarray.

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KDM4B regulates alternative splicing in castration resistant prostate cancer

Project description:KDM4B regulates alternative splicing in castration resistant prostate cancer

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Project description:FoxA1 has been shown critical for prostate development and prostate-specific gene expression regulation. In addition to its well-established role as an AR pioneering factor,several studies have recently revealed significant AR binding events in prostate cancer cells with FoxA1 knockdown. Furthermore, the role of FoxA1 itself in prostate cancer has not been carefully examined. Thus, it is important to understand the role of FoxA1 in prostate cancer and how it interacts with AR signaling. To address these questions, we generated engineered LNCaP cells with FoxA1 knockdown using shRNA or siRNA, 22RV1 cells with stable FoxA1 knockdown and PC3M cells with FoxA1 stable overexpression. We performed microarray analysis of these cells. We performed microarray analysis on LNCaP cells with FoxA1 knockdown using shRNA or siRNA, 22RV1 cells with stable FoxA1 knockdown and PC3M cells with FoxA1 stable overexpression

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Androgen receptor-independent function of FoxA1 in prostate cancer metastasis

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