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Blocking autophagy enhanced cytotoxicity induced by recombinant human arginase in triple-negative breast cancer cells

Z Wang1, X Shi2, Y Li2

  • 11] Department of Biosynthesis and Key Lab of Smart Drug Delivery of MOE, School of Pharmacy, Fudan University, Shanghai, China [2] Department of Biopharmaceutical Research, Shanghai Institute of Pharmaceutical Industry, Shanghai, China.

Cell Death & Disease
|December 16, 2014
PubMed

Insights

Recombinant human arginase (rhArg) inhibits triple-negative breast cancer (TNBC) cell growth. Autophagy plays a protective role, and inhibiting it enhances rhArg

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Triple-negative breast cancer (TNBC) lacks specific targets, leading to poor prognosis.
  • Recombinant human arginase (rhArg) is a promising cancer therapeutic by depleting arginine.
  • Investigating novel therapeutic strategies for TNBC is crucial.

Purpose of the Study:

  • To evaluate the cytotoxicity of rhArg against five TNBC cell lines.
  • To elucidate the role of autophagy in rhArg-induced cell death in TNBC.
  • To explore the involvement of reactive oxygen species (ROS) in rhArg's mechanism.

Main Methods:

  • Treatment of five TNBC cell lines with rhArg.
  • Assessment of cell viability and growth inhibition.
  • Analysis of autophagosome accumulation and autophagic flux.
  • Inhibition of autophagy using chloroquine (CQ), 3-methyladenine (3-MA), and Beclin1 siRNA.
  • Treatment with N-acetyl-l-cysteine (NAC) to investigate ROS involvement.

Main Results:

  • rhArg demonstrated significant inhibition of cell growth across all five TNBC cell lines.
  • rhArg treatment induced autophagosome accumulation and increased autophagic flux in MDA-MB-231 cells.
  • Inhibiting autophagy with CQ, 3-MA, or Beclin1 siRNA significantly enhanced rhArg-induced cytotoxicity.
  • NAC blocked rhArg-induced autophagy, indicating a role for ROS in rhArg's cytotoxic effects.

Conclusions:

  • Autophagy acts as a cytoprotective mechanism against rhArg-induced cell death in TNBC.
  • ROS are essential mediators of rhArg's cytotoxic activity in TNBC.
  • rhArg, alone or combined with autophagy inhibitors, represents a potential novel therapeutic strategy for TNBC.

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