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AMPK activation-dependent autophagy compromises oleanolic acid-induced cytotoxicity in human bladder cancer cells

Yarong Song1, Peng Zhang1, Yadong Sun1

  • 1Department of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.

Oncotarget
|October 6, 2017
PubMed

Insights

Oleanolic acid (OA) triggers protective autophagy in bladder cancer cells, promoting survival. Inhibiting this autophagy enhances OA

Area of Science:

  • Cell Biology
  • Cancer Research
  • Pharmacology

Background:

  • Autophagy is a cellular process crucial for stress response and implicated in drug resistance.
  • Bladder cancer exhibits resistance to conventional therapies, necessitating novel treatment strategies.

Purpose of the Study:

  • To investigate the role of autophagy in oleanolic acid (OA)-induced cytotoxicity in bladder cancer cells.
  • To elucidate the signaling pathways involved in OA-mediated autophagy.

Main Methods:

  • Cell viability, proliferation, and apoptosis assays were performed on bladder cancer cell lines (T24 and EJ).
  • Autophagy was modulated using siRNA (ATG7), inhibitors (bafilomycin A1, 3-MA), and activators (rapamycin, AICAR).
  • AMP-activated protein kinase (AMPK) and mechanistic target of rapamycin (mTOR) signaling pathways were analyzed.

Main Results:

  • Oleanolic acid inhibited bladder cancer cell viability and proliferation while inducing apoptosis.
  • OA activated autophagy via the AMPK-mTOR-ULK1 signaling pathway.
  • Inhibiting autophagy or AMPK enhanced OA-induced cancer cell death, while autophagy or AMPK activators reduced OA's anti-cancer effects.

Conclusions:

  • Oleanolic acid induces protective autophagy in bladder cancer cells through the AMPK-mTOR-ULK1 pathway.
  • Combining oleanolic acid with autophagy inhibitors may represent a novel therapeutic approach for bladder cancer treatment.
Keywords:
AMPKautophagybladder cancercytotoxicityoleanolic acid

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