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Article

Mutated SPOP E3 Ligase Promotes 17βHSD4 Protein Degradation to Drive Androgenesis and Prostate Cancer Progression.

Cancer research - 1 Jul 2021

Shi Lei, Yan Yuqian, He Yundong, Yan Binyuan, Pan Yunqian, Orme Jacob J, Zhang Jun, Xu Wanhai, Pang Jun, Huang Haojie

Abstract excerpt

Molecular mechanisms underlying intratumoral androgenesis and aberrant androgen receptor (AR) activation in prostate cancer remain poorly understood. Here we demonstrate that ectopic expression of the E3 ubiquitin ligase adaptor speckle-type poxvirus and zinc finger domain protein (SPOP) stabilizes 17βHSD4. SPOP bound a functional substrate-binding consensus (SBC) motif 315RATST319 in 17βHSD4 and promoted...

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PMID: 33762355
DOI: 10.1158/0008-5472.CAN-20-3258

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Mutated SPOP E3 Ligase Promotes 17βHSD4 Protein Degradation to Drive Androgenesis and Prostate Cancer Progression.PMID 33762355Read ↗

Deregulation of SPOP in Cancer.Semantic proximity Read ↗

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

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

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

SPOP-mediated ubiquitination and degradation of PDK1 suppresses AKT kinase activity and oncogenic functions.Semantic proximity Read ↗

Prostate cancer-associated SPOP mutations lead to genomic instability through disruption of the SPOP-HIPK2 axis.Semantic proximity Read ↗

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

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

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