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Blocking AMPK/ULK1-dependent autophagy promoted apoptosis and suppressed colon cancer growth

Jing Liu1, Shuaiyu Long1, Huanan Wang2,3

  • 11College of Biology, Hunan University, Changsha, 410082 China.

Cancer Cell International
|December 25, 2019
PubMed
Abstract

Insights

NVP-BEZ235 induces autophagy via the AMPK/ULK1 pathway in colon cancer. Inhibiting this autophagy enhances apoptosis and suppresses tumor growth, suggesting a potential therapeutic strategy.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Mechanisms

Background:

  • Autophagy is a cellular degradation process with a controversial role in tumor development.
  • The precise molecular mechanisms linking autophagy, apoptosis, and cancer remain poorly understood.

Purpose of the Study:

  • To investigate the role of NVP-BEZ235-induced autophagy in colon cancer.
  • To explore the therapeutic potential of targeting autophagy in combination with NVP-BEZ235.

Main Methods:

  • Cell viability and apoptosis assays (CCK8, crystal violet, Hoechst, flow cytometry).
  • Western blotting to analyze AMPK and ULK1 expression.
  • In vivo tumor xenograft mouse model to assess NVP-BEZ235 and chloroquine (CQ) efficacy.

Main Results:

  • NVP-BEZ235 induced autophagy through the AMPK/ULK1 pathway in colon cancer cells.
  • Blocking autophagy (AMPK/ULK1 knockdown) enhanced NVP-BEZ235-induced apoptosis and inhibited proliferation.
  • The autophagy inhibitor chloroquine (CQ) synergistically enhanced NVP-BEZ235's antitumor effects in vivo.

Conclusions:

  • NVP-BEZ235 triggers AMPK/ULK1-dependent autophagy in colon cancer.
  • Targeting this autophagy pathway potentiates apoptosis and suppresses tumor growth.
  • Combination therapy with NVP-BEZ235 and CQ presents a promising therapeutic strategy for colon cancer.
Keywords:
ApoptosisAutophagyCQColon cancerNVP-BEZ235

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