Chaperone-mediated autophagy modulates Snail protein stability: implications for breast cancer metastasis

Mol Cancer. 2024 Oct 11;23(1):227. doi: 10.1186/s12943-024-02138-0.

Abstract

Breast cancer remains a significant health concern, with triple-negative breast cancer (TNBC) being an aggressive subtype with poor prognosis. Epithelial-mesenchymal transition (EMT) is important in early-stage tumor to invasive malignancy progression. Snail, a central EMT component, is tightly regulated and may be subjected to proteasomal degradation. We report a novel proteasomal independent pathway involving chaperone-mediated autophagy (CMA) in Snail degradation, mediated via its cytosolic interaction with HSC70 and lysosomal targeting, which prevented its accumulation in luminal-type breast cancer cells. Conversely, Snail predominantly localized to the nucleus, thus evading CMA-mediated degradation in TNBC cells. Starvation-induced CMA activation downregulated Snail in TNBC cells by promoting cytoplasmic translocation. Evasion of CMA-mediated Snail degradation induced EMT, and enhanced metastatic potential of luminal-type breast cancer cells. Our findings elucidate a previously unrecognized role of CMA in Snail regulation, highlight its significance in breast cancer, and provide a potential therapeutic target for clinical interventions.

Keywords: Breast cancer; Chaperone-mediated autophagy; EMT; Metastasis; Snail.

MeSH terms

  • Animals
  • Autophagy
  • Breast Neoplasms / genetics
  • Breast Neoplasms / metabolism
  • Breast Neoplasms / pathology
  • Cell Line, Tumor
  • Chaperone-Mediated Autophagy*
  • Epithelial-Mesenchymal Transition*
  • Female
  • HSC70 Heat-Shock Proteins / metabolism
  • Humans
  • Lysosomes* / metabolism
  • Mice
  • Neoplasm Metastasis
  • Protein Stability*
  • Proteolysis
  • Snail Family Transcription Factors* / metabolism
  • Triple Negative Breast Neoplasms / genetics
  • Triple Negative Breast Neoplasms / metabolism
  • Triple Negative Breast Neoplasms / pathology

Substances

  • HSC70 Heat-Shock Proteins
  • Snail Family Transcription Factors
  • SNAI1 protein, human