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BOP1 Promotes Prostate Cancer through the DUSP6/MAPK Pathway.

Xiaoqing Wu1, Zheng Jing1, Tianpu Huang1

  • 1Department of Radiotherapy, Central Hospital Affiliated to Shandong First Medical University, 250000 Jinan, Shandong, China.

Archivos Espanoles De Urologia
|September 8, 2023
PubMed
Summary

Block of proliferation 1 (BOP1) promotes prostate cancer (CaP) progression. BOP1 upregulates dual-specificity phosphatase 6 (DUSP6), activating the MAPK pathway, driving CaP development and metastasis.

Keywords:
BOP1DUSP6MAPKprostate cancer

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Nucleolar prominence is a key biomarker for prostate cancer (CaP).
  • The nucleolar protein block of proliferation 1 (BOP1) is implicated in CaP development and presents a potential therapeutic target.

Purpose of the Study:

  • To elucidate the underlying mechanism of BOP1 in prostate cancer progression.
  • To investigate the role of BOP1 in regulating cell viability, apoptosis, and metastasis in CaP.

Main Methods:

  • Assessed BOP1 expression in CaP tissues and PC3 cells.
  • Evaluated the impact of BOP1 on PC3 cell viability, apoptosis, and metastasis in vitro.
  • Analyzed the effect of BOP1 on the mitogen-activated protein kinase (MAPK) pathway and its regulation of dual-specificity phosphatase 6 (DUSP6).

Main Results:

  • BOP1 and DUSP6 were upregulated in CaP tissues and cells.
  • BOP1 inhibition reduced PC3 cell viability, induced apoptosis, and suppressed metastasis.
  • BOP1 knockout inhibited DUSP6 expression and the MAPK pathway; DUSP6 overexpression rescued these effects.

Conclusions:

  • BOP1 promotes CaP progression by upregulating DUSP6 and activating the MAPK pathway.
  • Targeting the BOP1/DUSP6/MAPK axis offers a potential therapeutic strategy for prostate cancer.