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Updated: Jan 31, 2026

Isolation of Cancer Stem Cells From Human Prostate Cancer Samples
07:16

Isolation of Cancer Stem Cells From Human Prostate Cancer Samples

Published on: March 14, 2014

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AMPK Promotes SPOP-Mediated NANOG Degradation to Regulate Prostate Cancer Cell Stemness

Xinbo Wang1, Jiali Jin2, Fangning Wan3

  • 1Tongji University Cancer Center, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai 200072, China; Shanghai Putuo People's Hospital, School of Medicine, Tongji University, Shanghai 200060, China; Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai 200241, China.

Developmental Cell
|January 1, 2019
PubMed

Insights

NANOG protein stability is regulated by SPOP-mediated degradation in prostate cancer (PCa). Mutations in SPOP or NANOG disrupt this process, increasing PCa stemness and worsening prognosis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Stem Cell Research

Background:

  • NANOG is crucial for maintaining embryonic stem cells (ESCs) and prostate cancer stem cells (CSCs).
  • The regulation of NANOG protein stability during prostate cancer progression remains unclear.

Purpose of the Study:

  • To elucidate the mechanism regulating NANOG protein stability in prostate cancer.
  • To investigate the role of SPOP and its interaction with NANOG in prostate cancer stemness.

Main Methods:

  • Investigated the degradation of NANOG by SPOP, a tumor suppressor in prostate cancer.
  • Analyzed the impact of cancer-associated mutations in SPOP and NANOG (S68Y) on NANOG degradation.
  • Explored the role of the AMPK-BRAF signaling pathway in controlling NANOG phosphorylation at Ser68.

Main Results:

  • SPOP mediates the degradation of NANOG in prostate cancer.
  • Mutations in SPOP or NANOG at Ser68 prevent SPOP-mediated degradation, enhancing prostate cancer stemness and leading to poor prognosis.
  • Phosphorylation of NANOG at Ser68 by the AMPK-BRAF axis inhibits SPOP-NANOG interaction, thus controlling NANOG stability.

Conclusions:

  • Discovered a novel mechanism of prostate cancer stemness regulation via phosphorylation-dependent control of NANOG stability.
  • Identified SPOP and the AMPK-BRAF-NANOG axis as potential therapeutic targets for prostate cancer.
Keywords:
AMPK-BRAF axisNANOGSPOPprostate cancer stem cellubiquitination

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