MiR-17-5p promotes cervical cancer cell proliferation and metastasis by targeting transforming growth factor-β receptor 2

Eur Rev Med Pharmacol Sci. 2018 Apr;22(7):1899-1906. doi: 10.26355/eurrev_201804_14712.


Objective: MicroRNAs (miRNAs) play critical roles in post-translational gene expression. The aim of the current study was to investigate the effects of miR-17-5p in cervical cancer.

Patients and methods: Fifteen clinical cervical cancer tissue samples, as well as their paired adjacent noncancerous tissues, were collected. The microarray was performed to identify differential miRNAs in cervical cancer. Luciferase reporter assay was conducted to identify the target gene of selected miRNA. SiHa was transfected with mimics, inhibitors as well as negative controls of miR-17-5p and Targeting Transforming Growth Factor-β Receptor 2 (TGFBR2) open reading frame or siRNA. Cell counting kit-8 (CCK-8) assay and transwell experiment were performed to detect the proliferation rate and metastasis, respectively. Western blotting and quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) analysis were used to analyze TGFBR2 expression. Balb/c nude mice were utilized to verify the effect of miR-17-5p in vivo.

Results: Microarray analysis identified miR-17-5p as our interesting miRNA, and luciferase reporter assay identified TGFBR2 as its target gene. MiR-17-5p overexpression significantly enhanced cervical cancer cell proliferation and metastasis. In-vivo study also verified that miR-17-5p overexpression stimulated cervical cancer growth.

Conclusions: MiR-17-5p enhances cervical cancer proliferation and metastasis via targeting TGFBR2. It is proposed that targeting miR-17-5p may be a promising therapeutic approach for cervical cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line, Tumor
  • Cell Proliferation
  • Female
  • Humans
  • Mice
  • Mice, Inbred BALB C
  • MicroRNAs / physiology*
  • Neoplasm Metastasis
  • Receptor, Transforming Growth Factor-beta Type II / genetics*
  • Uterine Cervical Neoplasms / etiology
  • Uterine Cervical Neoplasms / pathology*


  • MIRN17 microRNA, human
  • MicroRNAs
  • Receptor, Transforming Growth Factor-beta Type II
  • TGFBR2 protein, human