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Rho kinase 2 promotes epithelial-mesenchymal transition and proliferation in human prostate cancer PC-3 cells

Alamgir Hossain1, Aya Yamamura2, Md Junayed Nayeem3

  • 1Department of Physiology, Aichi Medical University, 1-1 Yazakokarimata, Nagakute, Aichi, 480-1195, Japan; Eukaryotic Gene Expression and Function Research Group, AS Tower, Beside Mimisuper Market, Probortok Circle, Chattogram, 4000, Bangladesh.

Journal of Pharmacological Sciences
|November 15, 2025
PubMed

Insights

Targeting Rho-kinase 2 (ROCK2) shows promise for treating castration-resistant prostate cancer. Inhibiting ROCK2 reversed cancer cell progression and reduced tumor growth, offering a potential new therapeutic strategy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Prostate cancer resistance to androgen deprivation therapy leads to castration-resistant prostate cancer (CRPC).
  • Limited therapeutic options exist for CRPC, highlighting the need for novel treatment strategies.
  • Rho kinases (ROCK1 and ROCK2) are implicated in cancer progression, but their therapeutic potential is underexplored.

Purpose of the Study:

  • To investigate the roles of ROCK1 and ROCK2 in prostate cancer cell proliferation and epithelial-mesenchymal transition (EMT).
  • To evaluate ROCK2 as a potential therapeutic target for CRPC.

Main Methods:

  • Compared ROCK1 and ROCK2 expression in prostate epithelial cells and CRPC cell lines (PC-3, DU145).
  • Analyzed EMT markers (E-cadherin, N-cadherin, Snail) in PC-3 cells.
  • Utilized ROCK2 knockdown and a selective ROCK2 inhibitor (KD025) to assess effects on cell proliferation, migration, and spheroid formation.
  • Evaluated ROCK2 deficiency in a PC-3 xenograft mouse model.

Main Results:

  • ROCK2 expression was significantly higher in PC-3 cells compared to normal prostate cells and DU145 cells.
  • PC-3 cells exhibited an EMT phenotype (decreased E-cadherin, increased N-cadherin and Snail).
  • ROCK2 knockdown and KD025 treatment reversed EMT, reduced cell proliferation, migration, and spheroid viability, and attenuated tumor growth in vivo.

Conclusions:

  • ROCK2 promotes EMT and tumor progression in androgen-independent prostate cancer cells.
  • Targeting ROCK2, potentially with selective inhibitors like KD025, represents a promising therapeutic strategy for CRPC.
Keywords:
Epithelial-mesenchymal transitionKD025PC-3Prostate cancerROCK2

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