Up-regulation of miR-190b promoted growth, invasion, migration and inhibited apoptosis of Wilms' tumor cells by repressing the PTEN expression

Eur Rev Med Pharmacol Sci. 2018 Feb;22(4):961-969. doi: 10.26355/eurrev_201802_14377.

Abstract

Objective: Wilms' tumor (WT) is the most common malignant tumor in the children's urogenital system. MiR-190b was found to participate in the development and progression of several cancers. However, the molecular mechanism of miR-190b in WT is still unclear.

Patients and methods: We detected the miR-190b in WT tissue samples compared to adjacent normal samples as well as in WT patients' blood sample compared to normal volunteers using qRT-PCR. With over-expression and knockdown of miR-190b in WT-derived cell line SK-NEP-1, we next studied cell proliferation, cell circle, apoptosis, invasion and migration abilities change caused by miR-190b ectopic expression. Dual-luciferase assay and Western-blot analysis were used to explain the mechanism of miR-190b in WT.

Results: MiR-190b was over-expressed in WT tissue and blood samples compared to normal group, relatively. Up-regulation of miR-190b in SK-NEP-1 cells significantly increased the growth and decreased the apoptosis of cells, while its down-regulation reduced cell proliferation and promoted cell apoptosis of SK-NEP-1. Also, cell invasion and migration abilities were significantly improved after miR-190b over-expression. Moreover, PTEN was proved to be a direct target of miR-190b and its protein level was remarkably decreased after miR-190b up-regulation.

Conclusions: miR-190b over-expressed in WT and promoted cell proliferation, invasion and migration while reduced cell apoptosis of WT cells by repressing PTEN repression, which might provide a potential target for WT diagnosis and therapy.

MeSH terms

  • Apoptosis / physiology
  • Cell Line, Tumor
  • Cell Movement / physiology*
  • Cell Proliferation / physiology
  • Child, Preschool
  • Female
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Infant
  • Infant, Newborn
  • Kidney Neoplasms / genetics
  • Kidney Neoplasms / metabolism*
  • Kidney Neoplasms / pathology
  • Male
  • MicroRNAs / biosynthesis*
  • MicroRNAs / genetics
  • Neoplasm Invasiveness / pathology
  • PTEN Phosphohydrolase / antagonists & inhibitors
  • PTEN Phosphohydrolase / biosynthesis*
  • PTEN Phosphohydrolase / genetics
  • Up-Regulation / physiology
  • Wilms Tumor / genetics
  • Wilms Tumor / metabolism*
  • Wilms Tumor / pathology

Substances

  • MIRN190 microRNA, human
  • MicroRNAs
  • PTEN Phosphohydrolase
  • PTEN protein, human