These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Deregulation of the miR-16-KRAS axis promotes colorectal cancer.
    Author: You C, Liang H, Sun W, Li J, Liu Y, Fan Q, Zhang H, Yue X, Li J, Chen X, Ba Y.
    Journal: Sci Rep; 2016 Nov 18; 6():37459. PubMed ID: 27857191.
    Abstract:
    KRAS plays a significant role in the etiology and progression of colorectal cancer (CRC), but the mechanism underlying this process has not been fully elucidated. In this study, we found that the KRAS protein levels were higher in CRC tissues than in the normal adjacent tissues, whereas its mRNA levels varied irregularly, suggesting that a post-transcriptional mechanism is involved in the regulation of KRAS. Then, we performed bioinformatic analyses to search for miRNAs that potentially target KRAS. We predicted and experimentally validated that miR-16 directly recognizes the 3'-UTR of the KRAS transcript and regulates KRAS expression. Furthermore, the in vitro results showed that the repression of KRAS by miR-16 suppressed the proliferation and invasion and induced the apoptosis of CRC cells, and the in vivo results revealed that miR-16 exerted a tumor-suppressive effect by negatively regulating KRAS in xenograft mice. Taken together, our findings provide evidence supporting the role of miR-16 as a tumor suppressor in CRC by targeting KRAS.
    [Abstract] [Full Text] [Related] [New Search]