High expression of piwi-like RNA-mediated gene silencing 1 is associated with poor prognosis via regulating transforming growth factor-β receptors and cyclin-dependent kinases in breast cancer

Mol Med Rep. 2016 Mar;13(3):2829-35. doi: 10.3892/mmr.2016.4842. Epub 2016 Feb 2.

Abstract

Previous studies have demonstrated that abnormal expression levels of PIWI may serve a crucial role in tumorigenesis. However, the pathological role and its association with prognosis remains to be fully elucidated. In the present study, the expression levels of piwi‑like RNA‑mediated gene silencing 1 (HIWI) and piwi‑like RNA‑mediated gene silencing 2 (HILI) in breast cancer tissues were reported to be high. The high expression levels of HIWI are correlated with poor prognosis in detected patients. In addition, by overexpression and interference, it was demonstrated that HIWI promotes the activity of breast cancer cells while depression of HIWI may induce apoptosis of breast cancer cells. It was additionally identified that suppression of HIWI may arrest the cells at the G2/M stage. The expression levels of transforming growth factor‑β receptor (TβR)I, TβRII, cyclin‑dependent kinase (CDK)4, CDK6 and CDK8 were observed to be regulated by HIWI, which indicated a novel mechanism of HIWI in the regulation of breast cancer progression. The present study provides novel insight into the HIWI expression in breast cancer, providing a potential biomarker for assessment of prognosis and therapy of breast cancer.

MeSH terms

  • Adult
  • Argonaute Proteins / genetics
  • Argonaute Proteins / metabolism*
  • Breast Neoplasms / enzymology*
  • Breast Neoplasms / mortality
  • Cyclin-Dependent Kinases
  • Female
  • Gene Expression
  • Gene Expression Regulation, Neoplastic
  • Humans
  • MCF-7 Cells
  • Middle Aged
  • Prognosis
  • Proportional Hazards Models
  • RNA Interference
  • Receptors, Transforming Growth Factor beta / genetics
  • Receptors, Transforming Growth Factor beta / metabolism*

Substances

  • Argonaute Proteins
  • PIWIL1 protein, human
  • Receptors, Transforming Growth Factor beta
  • Cyclin-Dependent Kinases