Mir-139 Regulates Autophagy in Prostate Cancer Cells Through Beclin-1 and mTOR Signaling Proteins

Anticancer Res. 2020 Dec;40(12):6649-6663. doi: 10.21873/anticanres.14689. Epub 2020 Dec 7.

Abstract

Background/aim: We previously identified a panel of five miRNAs (including miR-139) associated with biochemical recurrence and metastasis in prostate cancer patients.

Materials and methods: We examined miR-139 transfected PC3, DU145 and LNCaP cells by morphology as well as by cell-based assays, confocal microscopy and immunoblotting.

Results: We found that treatment of prostate cancer cells with miR-139 resulted in phenotypic changes characteristic of autophagic cells. MiR-139 increased the autophagy-related conversion of the microtubule-associated protein light chain 3 (LC3-I to LC3-II) that was specifically inhibited by the miR-139 antagomir. The upregulation of LC3 II was further confirmed by confocal microscopy. miR-139 regulated activation of both mTOR and Beclin1 the two important autophagy-related molecules. We found that upon miR-139 treatment, the cargo adaptor protein p62 which is degraded during autophagy, accumulates.

Conclusion: These results suggest that miR-139 is inducing autophagic flux blockade leading to apoptosis in prostate cancer cells through the mTOR and Beclin-1 proteins.

Keywords: Beclin-1; LC3B-II; SQSTM1; apoptosis; autophagy; chloroquine; mTOR; miR-139; prostate cancer.

MeSH terms

  • Apoptosis / genetics
  • Autophagy / genetics*
  • Beclin-1 / metabolism*
  • Cell Line, Tumor
  • Cell Shape / genetics
  • Down-Regulation / genetics
  • Gene Expression Regulation, Neoplastic
  • Humans
  • MAP Kinase Signaling System
  • Male
  • MicroRNAs / metabolism*
  • Phosphatidylinositol 3-Kinases / metabolism
  • Prostatic Neoplasms / genetics*
  • Prostatic Neoplasms / pathology*
  • Proto-Oncogene Proteins c-akt / metabolism
  • Signal Transduction*
  • TOR Serine-Threonine Kinases / metabolism*
  • Up-Regulation / genetics

Substances

  • Beclin-1
  • MIRN139 microRNA, human
  • MicroRNAs
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases