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Autophagy deficiency promotes lung metastasis of prostate cancer via stabilization of TWIST1

Y X Shi1,2, Z W Sun3, D L Jia1,2

  • 1Department of Orthopaedics, Affiliated Hospital of Jining Medical University, No. 129 Hehua Road, Jining, Shandong, China.

Clinical & Translational Oncology : Official Publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
|February 8, 2022
PubMed
Abstract

Insights

Autophagy-related gene ATG5 controls prostate cancer metastasis by regulating p62 and TWIST1. Loss of ATG5 promotes metastasis via TWIST1 stabilization, while its presence inhibits it.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Mechanisms

Background:

  • The role of autophagy in prostate cancer metastasis is debated.
  • The specific influence of the autophagy-related gene ATG5 on prostate cancer metastasis is not well understood.

Purpose of the Study:

  • To investigate the impact of ATG5 on prostate cancer metastasis.
  • To elucidate the underlying molecular mechanisms by which ATG5 affects metastasis.

Main Methods:

  • Assessed metastatic characteristics using NOD/SCID mouse experiments, western blot, Transwell, and wound-healing assays.
  • Evaluated autophagic activity with double membrane vesicle observation and mCherry-GFP-LC3B fusion protein.
  • Confirmed the role of p62 in TWIST1 accumulation and ATG5's function in metastasis via lentiviral shATG5 interference.

Main Results:

  • p62 stabilizes TWIST1, influencing epithelial-mesenchymal transition (EMT) and prostate cancer metastasis.
  • Loss of ATG5 led to autophagy deficiency, p62 accumulation, TWIST1 stabilization, and increased metastasis in DU145 cells.
  • LNCaP cells with normal ATG5 expression exhibited limited metastatic potential, with similar findings in ATG5-interfered cells.

Conclusions:

  • ATG5-mediated autophagy is crucial for controlling prostate cancer metastasis.
  • This regulation occurs through modulating p62 levels and TWIST1 protein stability.
Keywords:
ATG5MetastasisPhenotype crosstalkTWIST1p62 accumulation

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