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Coptisine regulates PI3K/AKT pathway to block bladder cancer progression: a study based on network pharmacology, in

Yu Xiaohui1, Li Jie1,2, Zhou Jiangqiao3,4

  • 1Department of Vascular Surgery, Renmin Hospital of Wuhan University, Wuhan, China.

Hereditas
|November 25, 2025
PubMed
Abstract

Insights

Coptisine (COP) inhibits bladder cancer progression by targeting key proteins like AKT1 and GSK3B, thereby repressing the PI3K/AKT pathway. This natural compound shows promise in suppressing tumor growth and metastasis.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Coptisine (COP), a natural compound from Rhizoma Coptidis, exhibits inhibitory effects on bladder cancer.
  • The precise molecular mechanisms underlying COP's anti-cancer activity require further elucidation.

Purpose of the Study:

  • To investigate the downstream molecular mechanisms by which Coptisine (COP) exerts its therapeutic effects on bladder cancer.

Main Methods:

  • Utilized multiple databases (SwissTargetPrediction, STITCH, etc.) to identify COP and bladder cancer targets.
  • Constructed protein-protein interaction networks and performed molecular docking to identify hub targets.
  • Investigated COP's effect on the PI3K/AKT pathway via western blotting and validated anti-tumor properties in vivo.

Main Results:

  • Identified AKT1, GSK3B, CASP3, TNF, and CCND1 as key targets of COP in bladder cancer.
  • Confirmed high binding affinities between COP and these hub targets.
  • Demonstrated that COP inhibits the PI3K/AKT pathway, reducing tumor growth and metastasis in vivo.

Conclusions:

  • Coptisine (COP) acts as a natural inhibitor of AKT1, GSK3B, CASP3, TNF, and CCND1.
  • COP suppresses bladder cancer progression by inhibiting the PI3K/AKT signaling pathway.
Keywords:
Bladder cancerCoptisineMolecular dockingNetwork pharmacologyPI3K/AKT pathway

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