TargetRx Atlas

MRNA basic information

  • mRNA ID:ENST00000379561
  • Gene Name:FOXO1
  • mRNA database:Ensembl
  • mRNA expression :up-regulated
  • mRNA Method:qRT-PCR
  • mRNA Pathway:PTEN/Akt/FOXO1
  • Evidence:predicted
  • (mRNA-drug)

Drug basic information

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

Disease basic infommation

  • Disease:cervical cancer
  • Tissue:A human normal cervical epithelium cell line (End1/E6E7)

Other information

  • Title:Inhibition of microRNA-181a may suppress proliferation and invasion and promote apoptosis of cervical cancer cells through the PTEN/Akt/FOXO1 pathway.
  • Journal:J Physiol Biochem
  • Published:2016
  • PubMed ID:27534652
  • Abstract:MicroRNAs (miRNAs) are endogenous, non-coding, small RNAs, which play a critical role in regulating varieties of the biological and pathologic processes. miR-181a has been reported to participate in tumorigenic progression. However, the roles of miR-181a in cervical cancer (CC) are still unknown. The aim of this research was to explore the effects and molecular mechanism of miR-181a in CC cells. In this paper, the levels of miR-181a in CC cell lines were determined by real-time PCR. We found that the levels of miR-181a were evidently enhanced in CC cell lines compared with normal cervical epithelium cells. Then, the miR-181a inhibitor was transiently transfected into HeLa and CaSKi cells using Lipofectamine 2000 reagent. Subsequently, the Cell Counting Kit-8 (CCK-8) and BrdU-ELISA results showed that down-regulation of miR-181a inhibited the cell viability and proliferation. Our data also demonstrated that miR-181a inhibitor arrested cell cycle progression of HeLa and CaSKi cells by up-regulation of p21 and p27 expressions. In addition, inhibition of miR-181a promoted apoptosis of HeLa and CaSKi cells due to increasing Bax expression and decreasing Bcl-2 expression. Ultimately, the effect of miR-181a inhibitor on the PTEN/Akt/FOXO1 signaling pathway was investigated by Western blot. From our results, down-regulation of miR-181a increased the expression of PTEN and decreased phosphorylation of Akt and FOXO1. Altogether, miR-181a might be an oncogene in CC cells. The potential mechanism was that inhibition of miR-181a might suppress proliferation and invasion and promote apoptosis of HeLa and CaSKi cells by modulating the PTEN/Akt/FOXO1 signaling pathway.
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