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Novel insights into how autophagy regulates tumor cell motility

Erin E Mowers1,2,3, Marina N Sharifi1,2,4, Kay F Macleod1,4

  • 1a The Ben May Department for Cancer Research , University of Chicago , Chicago , IL , USA.

Autophagy
|July 22, 2016
PubMed

Insights

Autophagy promotes cancer metastasis by regulating focal adhesion disassembly. The protein paxillin binds to LC3B, facilitating cell movement and invasion, a process enhanced by oncogenic SRC.

Area of Science:

  • Cell Biology
  • Cancer Research
  • Molecular Biology

Background:

  • Metastasis is a complex process requiring tumor cells to adapt to new microenvironments.
  • Macroautophagy/autophagy is increasingly recognized for its role in cancer metastasis.
  • Increased autophagic flux is observed in distant metastases compared to primary tumors.

Purpose of the Study:

  • To investigate the role of autophagy in tumor cell motility.
  • To identify the mechanisms by which autophagy influences focal adhesion turnover.
  • To explore the interaction between autophagy proteins and focal adhesion components.

Main Methods:

  • Investigated the turnover of focal adhesions, critical for cell migration.
  • Identified the interaction between the focal adhesion protein paxillin (PXN) and LC3B.
  • Utilized the LC3-interacting region (LIR) motif for binding analysis.
  • Assessed the impact of oncogenic SRC on this interaction.

Main Results:

  • Autophagy plays a role in tumor cell motility through focal adhesion turnover.
  • Paxillin directly binds to LC3B via a conserved LIR motif.
  • This interaction promotes focal adhesion disassembly, enhancing metastasis.
  • Oncogenic SRC further promotes the paxillin-LC3B interaction.

Conclusions:

  • Autophagy, via paxillin-LC3B interaction, is a key regulator of focal adhesion disassembly and cancer metastasis.
  • Targeting this pathway could offer new therapeutic strategies for inhibiting cancer spread.
Keywords:
SRCautophagycell motilityfocal adhesionmetastasispaxillin

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