Loss of ARID1A accelerates prostate tumourigenesis with a proliferative collagen-poor phenotype through co-operation with AP1 subunit cFos.

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Tác giả: Imran Ahmad, Karen Blyth, Laura C A Galbraith, Andrew Hartley, Rakesh Heer, Hing Leung, Robin Shaw, Amy Tibbo, Rajan Veeratterapillay, Laura Wilson

Ngôn ngữ: eng

Ký hiệu phân loại:

Thông tin xuất bản: England : British journal of cancer , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 721323

BACKGROUND: Prostate cancer (PC) is the commonest male visceral cancer, and second leading cause of cancer mortality in men in the Western world. METHODS: Using a forward-mutagenesis Sleeping Beauty (SB) transposon-based screen in a Probasin Cre-Recombinase (Pb-Cre) Pten-deficient mouse model of PC, we identified Arid1a loss as a driver in the development of metastatic disease. RESULTS: The insertion of transposon in the Arid1a gene resulted in a 60% reduction of Arid1a expression, and reduced tumour free survival (SB:Pten CONCLUSION: Our data revealed homozygous Arid1a loss is required to dramatically accelerate prostate tumourigenesis. Analysis of RNA and ChIP -Sequencing data suggests Arid1a loss enhanced the function of AP-1 subunit cFos. In clinical PC cohort, ARID1A and cFos levels stratified an aggressive subset of PC with a poor survival outcome with a median of only 30 months.
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