TargetRx Atlas

MRNA basic information

  • mRNA ID:ENST00000257770
  • Gene Name:NT5E
  • mRNA database:Ensembl
  • mRNA expression :up-regulated
  • mRNA Method:qRT-PCR
  • mRNA Pathway:NA
  • Evidence:predicted
  • (mRNA-drug)

Drug basic information

  • Drug ID:NA
  • Drug Name:NA
  • Drug Method:NA

Disease basic infommation

  • Disease:prostate cancer
  • Tissue:Human PC cell lines (LNCaP, VCaP, DU145, and PC3) and a normal prostate epithelium cell line RWPE

Other information

  • Title:Tumor-Suppressive Function of miR-30d-5p in Prostate Cancer Cell Proliferation and Migration by Targeting NT5E
  • Journal:Cancer Biother Radiopharm
  • Published:2018
  • PubMed ID:29916747
  • Abstract:MiR-30d-5p, a member of the microRNA family, was recently reported to regulate androgen receptor signaling in prostate cancer (PCa). Ecto-5＇-nucleotidase (NT5E/CD73) is a pivotal regulator of tumor migration and has angiogenetic properties. However, the undiscovered function of miR-30d-5p and whether it targeted NT5E in PCa remain uncertain. In this study, the authors observed miR-30d-5p was significantly downregulated in PCa tissues and cell lines compared with the adjacent normal tissues and normal prostate cells, respectively. The lower expression of miR-30d-5p was found to be inversely correlated with the NT5E expression in PCa tissues. Subsequently, the biological function of miR-30d-5p was evaluated in PCa in vitro. The results indicated that miR-30d-5p overexpression inhibited PCa cell growth and invasion by MTT, Transwell assays, respectively, as well as induced cell cycle G0/G1 phase arrest and apoptosis using flow cytometry analysis. In addition, miR-30d-5p directly bound to the 3＇UTR (3＇ untranslated region) of NT5E in DU-145 and PC-3 cells by luciferase reporter assay. Furthermore, enforced NT5E expression alleviated miR-30d-5p inhibition of PCa cell growth and invasion in DU145 cells. Taken together, these data indicated that miR-30d-5p may be a potential therapeutic target for the treatment of PCa by serving as a tumor suppressor, by negatively regulating NT5E.
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