Transcriptomics

Dataset Information

0

Increased translation driven by a non-canonical EZH2 cistrome creates a synthetic vulnerability in enzalutamide-resistant prostate cancer (RNA-Seq polysome)


ABSTRACT: Resistance to therapy is a major challenge in castration-resistant prostate cancer (CRPC). Lineage plasticity towards a neuroendocrine phenotype enables CRPC to adapt and survive targeted-therapies. However, the molecular mechanisms of epigenetic reprogramming during this process are still poorly understood. Here we show that the protein kinase PKCl/i phosphorylates the epigenetic regulator enhancer of zeste homologue 2 (EZH2) to regulate its proteasomal degradation and maintain EZH2 as part of the canonical polycomb repressive complex (PRC2). Loss of PKCl/i promotes a switch during enzalutamide treatment to a non-canonical EZH2 cistrome that triggers the transcriptional activation of the translational machinery to induce a transforming growth factor b (TGFb) resistance program. The increased reliance on protein synthesis creates a synthetic vulnerability in PKCl/i-deficient CRPC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE266954 | GEO | 2024/10/22

REPOSITORIES: GEO

Dataset's files

Source:
Action DRS
Other
Items per page:
1 - 1 of 1

Similar Datasets

2024-10-22 | GSE266949 | GEO
2024-10-22 | GSE266955 | GEO
2024-10-22 | GSE266951 | GEO
2024-10-22 | GSE266950 | GEO
2024-10-22 | GSE272471 | GEO
2024-05-07 | MSV000094705 | MassIVE
2024-05-07 | MSV000094706 | MassIVE
2024-05-07 | MSV000094704 | MassIVE
2022-08-29 | GSE205106 | GEO
2022-08-29 | GSE205105 | GEO