MiR-769-5p, Which Targets HDGF , Inhibits Cell Proliferation and Invasion in Nonsmall Cell Lung Cancer.

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  • Author(s): Sun Y;Sun Y;Sun Y; Li J; Li J; Zheng S; Zheng S
  • Source:
    Cancer biotherapy & radiopharmaceuticals [Cancer Biother Radiopharm] 2021 Dec 31. Date of Electronic Publication: 2021 Dec 31.
  • Publication Type:
    Journal Article
  • Language:
    English
  • Additional Information
    • Publication Information:
      Ahead of Print
    • Source:
      Publisher: Mary Ann Liebert, Inc Country of Publication: United States NLM ID: 9605408 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1557-8852 (Electronic) Linking ISSN: 10849785 NLM ISO Abbreviation: Cancer Biother Radiopharm Subsets: MEDLINE
    • Publication Information:
      Original Publication: Larchmont, NY : Mary Ann Liebert, Inc., c1996-
    • Abstract:
      MiR-769-5p regulates tumor correlative genes, which plays a critical role in the progression of various types of tumor. However, the precise regulatory mechanism of miR-769-5p on nonsmall cell lung cancer (NSCLC) is unknown. This study was to discover the role and underlying mechanisms of miR-769-5p in NSCLC. MiR-769-5p expression was shown to be reduced, according to our findings. MiR-769-5p overexpression inhibited NSCLC cell proliferation while promoting NSCLC cell apoptosis. Furthermore, NSCLC cell migration and invasion were reduced when miR-769-5p was overexpressed. Furthermore, HDGF was confirmed as a miR-769-5p target gene that was negatively regulated by miR-769-5p. Furthermore, more research revealed that HDGF overexpression reduced the inhibitory effect of miR-769-5p on NSCLC cell biofunction. Finally, miR-769-5p inhibited NSCLC cell proliferation and invasion by targeting HDGF , indicating that NSCLC could benefit from miR-769-5p as a diagnostic and prognostic biomarker.
    • Contributed Indexing:
      Keywords: HDGF; NSCLC; antitumor function; miR-769-5p
    • Publication Date:
      Date Created: 20220103 Latest Revision: 20240220
    • Publication Date:
      20240220
    • Accession Number:
      10.1089/cbr.2021.0363
    • Accession Number:
      34978893