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Updated: Feb 9, 2026

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Targeting PRPK and TOPK for skin cancer prevention and therapy

Eunmiri Roh1, Mee-Hyun Lee1,2, Tatyana A Zykova1

  • 1The Hormel Institute, University of Minnesota, Austin, MN, 55912, USA.

Oncogene
|June 16, 2018
PubMed

Insights

Targeting p53-related protein kinase (PRPK) may prevent skin cancer. Inhibiting PRPK with rocuronium bromide or betamethasone reduced solar ultraviolet-induced skin tumors in mice.

Area of Science:

  • Oncology
  • Dermatology
  • Molecular Biology

Background:

  • Solar ultraviolet (sUV) irradiation is a primary environmental carcinogen causing skin inflammation and cancer.
  • Rising skin cancer rates necessitate identifying novel preventative molecules.
  • p53-related protein kinase (PRPK) is implicated in oncogenesis.

Purpose of the Study:

  • To investigate the role of PRPK in solar-simulated light (SSL)-induced skin carcinogenesis.
  • To evaluate the therapeutic potential of PRPK inhibitors against skin cancer.

Main Methods:

  • Identified PRPK as a novel oncogenic protein phosphorylated by T-LAK cell-originated protein kinase (TOPK).
  • Utilized mouse models to assess the effects of TOPK knockdown and PRPK inhibitors on SSL-induced skin carcinogenesis.
  • Analyzed human skin tissues post-SSL irradiation to examine TOPK and PRPK expression.

Main Results:

  • Knockdown of TOPK inhibited PRPK phosphorylation and conferred resistance to SSL-induced skin carcinogenesis.
  • SSL irradiation increased epidermal thickness and TOPK/PRPK levels in human skin.
  • Rocuronium bromide and betamethasone attenuated TOPK-dependent PRPK signaling, reducing tumor development and proliferation markers in mice.

Conclusions:

  • PRPK is a novel oncogenic protein activated by TOPK in response to sUV irradiation.
  • Targeting PRPK with FDA-approved drugs like rocuronium bromide or betamethasone shows promise in preventing sUV-induced skin cancer.
  • This study highlights PRPK as a potential therapeutic target for cutaneous squamous cell carcinoma (cSCC).

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