Mar 8, 2020

Role of Specialized mSWI/SNF Complexes in Prostate Cancer Lineage Plasticity

bioRxiv
Joanna CyrtaMark A Rubin

Abstract

Advanced prostate cancer initially responds to hormonal treatment, but ultimately becomes resistant and requires more potent therapies. One mechanism of resistance observed in ~10% of these patients is through lineage plasticity, which manifests in a partial or complete small cell or neuroendocrine prostate cancer (NEPC) phenotype. Here, we investigate the role of the mammalian SWI/SNF (mSWI/SNF) chromatin remodeling complex in NEPC. Using large patient datasets, patient-derived organoids and cancer cell lines, we identify mSWI/SNF subunits that are deregulated in NEPC and demonstrate that SMARCA4 (BRG1) overexpression is associated with aggressive disease. We also show that SWI/SNF complexes interact with different lineage-specific factors in NEPC compared to prostate adenocarcinoma. These data suggest a role for mSWI/SNF complexes in therapy-related lineage plasticity, which may be relevant for other solid tumors.

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Mentioned in this Paper

Adenocarcinoma of Prostate
Protein Overexpression
Malignant Neoplasm of Prostate
Solid Tumour
Drug Resistance
SMARCA4
Cell Line, Tumor
Complex (molecular entity)
Small Melanoma Cell
Organoids

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