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Nuclear Pores Promote Lethal Prostate Cancer by Increasing POM121-Driven E2F1, MYC, and AR Nuclear Import
Journal article   Open access   Peer reviewed

Nuclear Pores Promote Lethal Prostate Cancer by Increasing POM121-Driven E2F1, MYC, and AR Nuclear Import

Veronica Rodriguez-Bravo, Raffaella Pippa, Won-Min Song, Marc Carceles-Cordon, Ana Dominguez-Andres, Naoto Fujiwara, Jungreem Woo, Anna P. Koh, Adam Ertel, Ravi K. Lokareddy, …
Cell, v 174(5), pp 1200-1215
23 Aug 2018
PMID: 30100187
url
https://doi.org/10.1016/j.cell.2018.07.015View
Published, Version of Record (VoR)Open Access (Publisher-Specific) Open

Abstract

androgen receptor E2F1 GATA2 importin β MYC nuclear import nuclear pore nuclear transport POM121 prostate cancer
Nuclear pore complexes (NPCs) regulate nuclear-cytoplasmic transport, transcription, and genome integrity in eukaryotic cells. However, their functional roles in cancer remain poorly understood. We interrogated the evolutionary transcriptomic landscape of NPC components, nucleoporins (Nups), from primary to advanced metastatic human prostate cancer (PC). Focused loss-of-function genetic screen of top-upregulated Nups in aggressive PC models identified POM121 as a key contributor to PC aggressiveness. Mechanistically, POM121 promoted PC progression by enhancing importin-dependent nuclear transport of key oncogenic (E2F1, MYC) and PC-specific (AR-GATA2) transcription factors, uncovering a pharmacologically targetable axis that, when inhibited, decreased tumor growth, restored standard therapy efficacy, and improved survival in patient-derived pre-clinical models. Our studies molecularly establish a role of NPCs in PC progression and give a rationale for NPC-regulated nuclear import targeting as a therapeutic strategy for lethal PC. These findings may have implications for understanding how NPC deregulation contributes to the pathogenesis of other tumor types. [Display omitted] •Nuclear pores display a distinct Nup composition during progression to lethal PC•Nup POM121 impacts on PC aggressiveness by enhancing importin β function•POM121 promotes nuclear import of key transcription factors driving PC•Targeting the POM121-importin β axis decreases the aggressiveness of PC tumors POM121- and importin β-mediated nuclear import of a subset of oncogenic transcription factors promotes prostate cancer aggressiveness and reveals a pharmacologically targetable dependency.

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Collaboration types
Domestic collaboration
International collaboration
Web of Science research areas
Biochemistry & Molecular Biology
Cell Biology
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