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BEX2 regulates autophagy by inhibiting PIK3CA-p85 interaction in non-small-cell lung cancer cells

Yu Wang1,2, Ning Mu2, Xinke Wang3

  • 1Department of Pulmonary and Critical Care Medicine, Qilu Hospital of Shandong University, Jinan, 250012, China.

Cell Communication and Signaling : CCS
|December 15, 2025
PubMed
Abstract

Insights

BEX2 protein promotes autophagy by inhibiting the PI3K/AKT/mTOR pathway. This cancer cell survival mechanism involves BEX2 interacting with PIK3CA, hindering its activation and thus promoting autophagic flux.

Area of Science:

  • Cellular Biology
  • Cancer Research
  • Molecular Oncology

Background:

  • Autophagy is a crucial cellular process for maintaining homeostasis.
  • Tumor cells utilize autophagy for survival and drug resistance.
  • The PI3K/AKT/mTOR pathway is central to autophagy induction, while BEX2's role is unclear.

Purpose of the Study:

  • To investigate the function of BEX2 in autophagy.
  • To elucidate the mechanism by which BEX2 influences cancer cell autophagy and survival.

Main Methods:

  • Utilized human non-small cell lung cancer (NSCLC) cell lines and 293FT cells.
  • Employed western blot, co-immunoprecipitation, and confocal microscopy.
  • Analyzed BEX2 protein levels and its interaction with key signaling molecules.

Main Results:

  • Rapamycin treatment increased BEX2 protein levels.
  • BEX2 was found to regulate autophagy and impair PI3K/AKT/mTOR signaling.
  • BEX2 interacts with PIK3CA, inhibiting PI3K activity by disrupting the PIK3CA/p85 interaction.

Conclusions:

  • BEX2 promotes autophagic flux through the PI3K/AKT/mTOR pathway.
  • BEX2's interaction with PIK3CA hinders pathway activation, thereby promoting autophagy induction in cancer cells.
Keywords:
AutophagyBEX2NSCLCPIK3CA

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