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Adiponectin Receptor Agonist AdipoRon Inhibits Proliferation and Drives Glycolytic Dependence in Non-Small-Cell Lung

Sanober Kafeel1, Angela Ragone1, Alessia Salzillo1

  • 1Department of Precision Medicine, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy.

Cancers
|August 10, 2024
PubMed

Insights

AdipoRon, an adiponectin receptor agonist, demonstrates significant anticancer effects against non-small-cell lung cancer (NSCLC) by inhibiting cell viability and growth. It also impacts cancer cell metabolism, suggesting its potential as a novel NSCLC therapeutic agent.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Metabolism

Background:

  • Non-small-cell lung cancer (NSCLC) remains a leading cause of cancer mortality globally.
  • Conventional therapies show limited efficacy in advanced and non-oncogene addicted NSCLC.
  • AdipoRon, an adiponectin receptor agonist, exhibits antiproliferative effects in various cancer types.

Purpose of the Study:

  • To investigate the potential anticancer role of AdipoRon in non-small-cell lung cancer (NSCLC) for the first time.
  • To elucidate the mechanisms underlying AdipoRon's effects on NSCLC cells.

Main Methods:

  • Assessed AdipoRon's impact on NSCLC cell viability, growth, and colony formation (H1299 and A549 cell lines).
  • Analyzed cell cycle progression and metabolic switching (glucose consumption, lactate accumulation).
  • Investigated the role of AMP-activated protein kinase (AMPK) activation and glycolytic interference.

Main Results:

  • AdipoRon significantly inhibited NSCLC cell viability, growth, and colony formation.
  • AdipoRon induced cell cycle arrest and altered cellular metabolism, increasing glucose uptake and lactate production.
  • AdipoRon activated AMP-activated protein kinase (AMPK), and inhibiting this activation counteracted AdipoRon's effects.
  • Glycolytic inhibitors (2-Deoxy Glucose, Oxamate) enhanced AdipoRon's antiproliferative activity.

Conclusions:

  • AdipoRon exhibits potent anticancer properties against NSCLC cells.
  • AdipoRon's mechanism involves cell cycle slowdown, metabolic reprogramming, and AMPK activation.
  • AdipoRon shows promise as a potential therapeutic candidate for non-small-cell lung cancer treatment.
Keywords:
AMPKAdipoRonNSCLCglycolysis

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