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Autophagy induced by cardamonin is associated with mTORC1 inhibition in SKOV3 cells

Daohua Shi1, Peiguang Niu1, Xiaojie Heng1

  • 1Department of Pharmacy, Fujian Provincial Maternity and Children's Hospital, Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China.

Pharmacological Reports : PR
|August 13, 2018
PubMed
Abstract

Insights

Cardamonin inhibits cell viability and proliferation by inducing autophagy through mammalian target of rapamycin (mTOR) complex 1 (mTORC1) inhibition. This occurs via decreasing the regulatory associated protein of mTOR (Raptor) in SKOV3 cells.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Pharmacology

Background:

  • Mammalian target of rapamycin (mTOR) regulates cell proliferation and autophagy.
  • Cardamonin demonstrates anti-proliferative effects by inhibiting mTOR.

Purpose of the Study:

  • To investigate the effect of cardamonin on autophagy.
  • To elucidate the mechanism of cardamonin-induced mTOR inhibition.

Main Methods:

  • Cell viability and proliferation assays (MTT, BrdU).
  • Apoptosis and autophagy detection (flow cytometry, electron microscopy, GFP-LC3).
  • Mechanism investigation using Raptor siRNA and overexpression.

Main Results:

  • Cardamonin inhibited cell viability, proliferation, and induced apoptosis.
  • Cardamonin increased autophagosomes and LC3-II levels, indicating induced autophagy.
  • Cardamonin suppressed mTORC1 signaling by reducing Raptor protein and mTOR/S6K1 phosphorylation, without affecting mTORC2/Akt.
  • Raptor modulation affected cardamonin's inhibitory effects on mTORC1 and cell viability.

Conclusions:

  • Cardamonin induces autophagy via mTORC1 inhibition.
  • The mechanism involves a decrease in Raptor protein levels in SKOV3 cells.
Keywords:
AutophagyCardamoninOvarian cancerRaptormTOR

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