Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Intrinsic BET inhibitor resistance in SPOP-mutated prostate cancer is mediated by BET protein stabilization and AKT-mTORC1 activation.

Nature medicine - 1 Sept 2017

Zhang Pingzhao, Wang Dejie, Zhao Yu, Ren Shancheng, Gao Kun, Ye Zhenqing, Wang Shangqian, Pan Chun-Wu, Zhu Yasheng, Yan Yuqian, Yang Yinhui, Wu Di, He Yundong, Zhang Jun, Lu Daru, Liu Xiuping, Yu Long, Zhao Shimin, Li Yao, Lin Dong, Wang Yuzhuo, Wang Liguo, Chen Yu, Sun Yinghao, Wang Chenji, Huang Haojie

Abstract excerpt

Bromodomain and extraterminal domain (BET) protein inhibitors are emerging as promising anticancer therapies. The gene encoding the E3 ubiquitin ligase substrate-binding adaptor speckle-type POZ protein (SPOP) is the most frequently mutated in primary prostate cancer. Here we demonstrate that wild-type SPOP binds to and induces ubiquitination and proteasomal degradation of BET proteins (BRD2, BRD3 and BRD4) by...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Azepines
Share to Immunoprecipitation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mechanistic Target of Rapamycin Complex 1

Share to Multiprotein Complexes

Share to Proteasome Endopeptidase Complex

Share to rac1 GTP-Binding Protein

Share to TOR Serine-Threonine Kinases

Share to Triazoles

Source

Open in PubMed Open full text

Identifiers

PMID: 28805822
DOI: 10.1038/nm.4379
PMCID: PMC5653288

Genes

SPOP
BRD4
BRD2
BRD3
RAC1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Intrinsic BET inhibitor resistance in SPOP-mutated prostate cancer is mediated by BET protein stabilization and AKT-mTORC1 activation.PMID 28805822Read ↗

Destruction of DDIT3/CHOP protein by wild-type SPOP but not prostate cancer-associated mutants.Semantic proximity Read ↗

Re: Prostate Cancer-Associated SPOP Mutations Confer Resistance to BET Inhibitors through Stabilization of BRD4.Semantic proximity Read ↗

SPOP Gene Mutations in Prostate Cancer: Deciphering Their Role in Disease Characterization and Targeted Interventions on AR SignalingSemantic proximity Read ↗

Opposing effects of cancer-type-specific SPOP mutants on BET protein degradation and sensitivity to BET inhibitors.Semantic proximity Read ↗

Opposing Roles of SPOP Mutations in Human Prostate and Endometrial Cancers.Semantic proximity Read ↗

G3BP1 inhibits Cul3SPOP to amplify AR signaling and promote prostate cancer.Semantic proximity Read ↗

The novel BET‐CBP/p300 dual inhibitor NEO2734 is active in SPOP mutant and wild‐type prostate cancerSemantic proximity Read ↗

Deregulation of SPOP in Cancer.Semantic proximity Read ↗

Updates on SPOP Gene Mutations in Prostate Cancer and Computational Insights From TCGA cBioPortal DatabaseSemantic proximity Read ↗

Clinico-pathological significance of the molecular alterations of the SPOP gene in prostate cancer.Semantic proximity Read ↗

SPOP Mutations Target STING1 Signaling in Prostate Cancer and Create Therapeutic Vulnerabilities to PARP Inhibitor-Induced Growth Suppression.Semantic proximity Read ↗

SPOP promotes ATF2 ubiquitination and degradation to suppress prostate cancer progressionSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.