miR-19a promotes the metastasis and EMT through CUL5 in prostate cancer cell line PC3

J BUON. 2020 Jul-Aug;25(4):2028-2035.

Abstract

Purpose: Prostate cancer is an epithelial malignancy that occurs in the prostate and metastasis is a challenge of the treatment of prostate cancer. MicroRNA (miR)-19a was usually upregulated in several cancers at the roles of miR-19a in the metastasis in prostate cancer are still unclear.

Methods: A normal prostate epithelial cell line P69 and two prostate cancer cell lines PC3 and DU145 were used in this study. The mRNA levels of miR-19a and CUL5 were measured using qRT-PCR assay. Transwell and Western blot assays were conducted to calculate cell metastasis and epithelial-mesenchymal transition (EMT) properties in PC3 cells. Luciferase reporter assay was applied to validate that miR-19a targeted to CUL5.

Results: The expression of miR-19a was high in prostate cancer and its overexpression predicted poor outcome of prostate cancer patients. miR-19a regulated the expression of CUL5 by directly targeting its mRNA 3'-UTR in PC3 cells. The expression of CUL5 was lower in prostate cancer tissues and cell lines than in non-tumor tissues and normal cells. Downregulation of CUL5 predicted worse outcome of prostate cancer patients. miR-19a promoted cell migration, invasion and EMT in prostate cancer by directly binding to CUL5 mRNA 3'-UTR. CUL5 partially reversed the roles of miR-19a on the metastasis in prostate cancer.

Conclusion: miR-19a promoted migratory, invasive and EMT abilities by binding to CUL5 in prostate cancer. The newly identified miR-19a/CUL5 axis provides novel insight into the pathogenesis of prostate cancer.

MeSH terms

  • Cell Proliferation / physiology
  • Cullin Proteins / genetics
  • Cullin Proteins / metabolism*
  • Epithelial-Mesenchymal Transition
  • Humans
  • Male
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Neoplasm Metastasis
  • PC-3 Cells
  • Prostatic Neoplasms / genetics
  • Prostatic Neoplasms / metabolism*
  • Prostatic Neoplasms / pathology
  • Transfection

Substances

  • CUL5 protein, human
  • Cullin Proteins
  • MIRN19 microRNA, human
  • MicroRNAs