Loss of PTEN accelerates NKx3.1 degradation to promote prostate cancer progression

Cai Bowen, Michael C. Ostrowski, Gustavo Leone, Edward P. Gelmann

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

NKX3.1 is the most commonly deleted gene in prostate effect of PTEN on NKX3.1 was mediated via rapid enzyme–cancer and a gatekeeper suppressor. NKX3.1 is a growth substrate interaction. An effect of PTEN on Nkx3.1 gene suppressor, mediator of apoptosis, inducer of antioxidants, transcription was seen in vitro, but not in vivo. In gene- and enhancer of DNA repair. PTEN is a ubiquitous tumor targeted mice, Nkx3.1 expression significantly diminished suppressor that is often decreased in prostate cancer shortly after loss of Pten expression in the prostate. Nkx3.1 during tumor progression. Steady-state turnover of NKX3.1 loss primarily increased prostate epithelial cell proliferation is mediated by DYRK1B phosphorylation at NKX3.1 serine in vivo. In these mice, Nkx3.1 mRNA was not affected by Pten 185 that leads to polyubiquitination and proteasomal degra-expression. Thus, the prostate cancer suppressors PTEN and dation. In this study, we show PTEN is an NKX3.1 phosphatase NKX3.1 interact and loss of PTEN is responsible, at least in that protects NKX3.1 from degradation. PTEN specifically part, for progressive loss of NKX3.1 that occurs during tumor opposed phosphorylation at NKX3.1(S185) and prolonged progression. NKX3.1 half-life. PTEN and NKX3.1 interacted primarily in the nucleus as loss of PTEN nuclear localization abrogated its Significance: PTEN functions as a phosphatase of NKX3.1, a ability to bind to and protect NKX3.1 from degradation. The gatekeeper suppressor of prostate cancer.

Original languageEnglish (US)
Pages (from-to)4124-4134
Number of pages11
JournalCancer Research
Volume79
Issue number16
DOIs
StatePublished - Aug 15 2019
Externally publishedYes

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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