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ARAF regulates malignant progression of bladder cancer through the p38MAPK pathway

Xian Zhao1, Xiaojing Xu2

  • 1Department of Urology, Taikang Tongji (Wuhan) Hospital, Wuhan, China.

Open Medicine (Warsaw, Poland)
|May 28, 2026
PubMed
Abstract

Insights

Inhibition of A-Raf proto-oncogene serine/threonine kinase (ARAF) suppresses bladder cancer cell proliferation and metastasis. This occurs by repressing the p38 mitogen-activated protein kinase (MAPK) pathway, offering a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Bioinformatics

Background:

  • The A-Raf proto-oncogene serine/threonine kinase (ARAF) is implicated in bladder cancer development.
  • The mitogen-activated protein kinase (MAPK) pathway is frequently dysregulated in various cancers.

Purpose of the Study:

  • To investigate the role of ARAF in bladder cancer.
  • To elucidate the molecular mechanisms underlying ARAF's function in bladder cancer progression.

Main Methods:

  • Bioinformatic analysis of public databases (GeneCards, CTD) and KEGG pathway analysis.
  • Assessment of ARAF expression using RT-qPCR and Western blotting in bladder cancer cells.
  • Functional assays including EdU, flow cytometry, and Transwell assays to evaluate proliferation, apoptosis, migration, and invasion.

Main Results:

  • ARAF was identified as a key gene associated with bladder cancer and enriched in the p38MAPK pathway.
  • Elevated ARAF expression was observed in bladder cancer cells.
  • ARAF inhibition significantly reduced cell proliferation and metastasis, induced apoptosis, and suppressed p38MAPK pathway activation.

Conclusions:

  • ARAF plays a crucial role in promoting bladder cancer cell proliferation and metastasis.
  • Inhibiting ARAF offers a potential therapeutic strategy for bladder cancer by targeting the p38MAPK pathway.
Keywords:
ARAFapoptosisbladder cancerp38MAPK pathway

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