The novel BH-3 mimetic apogossypolone induces Beclin-1- and ROS-mediated autophagy in human hepatocellular carcinoma [corrected] cells

Cell Death Dis. 2013 Feb 7;4(2):e489. doi: 10.1038/cddis.2013.17.

Abstract

Apogossypolone (ApoG2), a novel derivative of gossypol, exhibits superior antitumor activity in Bcl-2 transgenic mice, and induces autophagy in several cancer cells. However, the detailed mechanisms are not well known. In the present study, we showed that ApoG2 induced autophagy through Beclin-1- and reactive oxygen species (ROS)-dependent manners in human hepatocellular carcinoma (HCC) cells. Incubating the HCC cell with ApoG2 abrogated the interaction of Beclin-1 and Bcl-2/xL, stimulated ROS generation, increased phosphorylation of ERK and JNK, and HMGB1 translocation from the nucleus to cytoplasm while suppressing mTOR. Moreover, inhibition of the ROS-mediated autophagy by antioxidant N-acetyl-cysteine (NAC) potentiates ApoG2-induced apoptosis and cell killing. Our results show that ApoG2 induced protective autophagy in HCC cells, partly due to ROS generation, suggesting that antioxidant may serve as a potential chemosensitizer to enhance cancer cell death through blocking ApoG2-stimulated autophagy. Our novel insights may facilitate the rational design of clinical trials for Bcl-2-targeted cancer therapy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylcysteine / pharmacology
  • Antineoplastic Agents / toxicity*
  • Antioxidants / pharmacology
  • Apoptosis Regulatory Proteins / antagonists & inhibitors
  • Apoptosis Regulatory Proteins / genetics
  • Apoptosis Regulatory Proteins / metabolism*
  • Autophagy / drug effects*
  • Beclin-1
  • Carcinoma, Hepatocellular / metabolism
  • Carcinoma, Hepatocellular / pathology
  • Cell Line, Tumor
  • Cyclin D1 / metabolism
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Gossypol / analogs & derivatives*
  • Gossypol / toxicity
  • HMGB1 Protein / metabolism
  • Hep G2 Cells
  • Humans
  • JNK Mitogen-Activated Protein Kinases / metabolism
  • Liver Neoplasms / metabolism
  • Liver Neoplasms / pathology
  • Membrane Proteins / antagonists & inhibitors
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism*
  • Microtubule-Associated Proteins / metabolism
  • Phosphorylation
  • RNA Interference
  • RNA, Small Interfering / metabolism
  • Reactive Oxygen Species / metabolism*
  • TOR Serine-Threonine Kinases / metabolism
  • bcl-X Protein / metabolism

Substances

  • Antineoplastic Agents
  • Antioxidants
  • Apoptosis Regulatory Proteins
  • BECN1 protein, human
  • Beclin-1
  • HMGB1 Protein
  • MAP1LC3A protein, human
  • Membrane Proteins
  • Microtubule-Associated Proteins
  • RNA, Small Interfering
  • Reactive Oxygen Species
  • apogossypolone
  • bcl-X Protein
  • Cyclin D1
  • TOR Serine-Threonine Kinases
  • Extracellular Signal-Regulated MAP Kinases
  • JNK Mitogen-Activated Protein Kinases
  • Gossypol
  • Acetylcysteine