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Targeting the anaphase promoting complex: common pathways for viral infection and cancer therapy

Linda Smolders1, Jose G Teodoro

  • 1McGill University, Goodman Cancer Research Centre, Department of Biochemistry, 1160 Pine Avenue West, Room 616, Montreal, Quebec H3A 1A3, Canada.

Expert Opinion on Therapeutic Targets
|March 8, 2011
PubMed
Abstract

Insights

Targeting the anaphase promoting complex/cyclosome (APC/C) offers a novel cancer therapy strategy. Viral interactions with APC/C reveal its potential for selective cancer cell elimination by exploiting tumour cell vulnerabilities.

Area of Science:

  • Cell Cycle Regulation
  • Cancer Therapeutics
  • Virology

Background:

  • The anaphase promoting complex/cyclosome (APC/C) is a ubiquitin ligase crucial for cell cycle control via substrate proteolysis.
  • Viral proteins often hijack APC/C function to manipulate cell cycle progression for replication.
  • APC/C inhibition by viruses can induce G(2)/M arrest and apoptosis, with some viruses selectively targeting tumor cells.

Purpose of the Study:

  • To review recent studies on viral APC/C interactions.
  • To highlight APC/C as a promising therapeutic target for cancer treatment.

Main Methods:

  • Literature review of viral APC/C interactions over the past decade.
  • Analysis of recent discoveries regarding APC/C in cancer therapy.

Main Results:

  • Viral proteins interact with APC/C, disrupting cell cycle regulation.
  • APC/C inhibition can lead to mitotic arrest and apoptosis, with potential for selective tumor cell killing.
  • Recent evidence suggests APC/C, particularly Cdc20, is a viable therapeutic target.

Conclusions:

  • Cancer cells exhibit increased dependency on APC/C function due to oncogenic transformation and mitotic stress.
  • Targeting APC/C, especially Cdc20, may overcome limitations of current therapies like spindle assembly checkpoint (SAC) activation.
  • APC/C inhibition presents a promising strategy for selective elimination of cancer cells, circumventing mitotic slippage observed in weakened SAC cancer cells.

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