Knockdown of LINC00467 contributed to Axitinib sensitivity in hepatocellular carcinoma through miR-509-3p/PDGFRA axis

Gene Ther. 2021 Nov;28(10-11):634-645. doi: 10.1038/s41434-020-0137-9. Epub 2020 Mar 27.

Abstract

Hepatocellular carcinoma (HCC) is a common histological class of primary liver cancer with dismal prognosis. Long noncoding RNAs (lncRNAs) are increasingly documented as participators in cancers. Present study aimed to explore the role of long intergenic nonprotein-coding RNA 467 (LINC00467) in HCC. LINC00467 was upregulated in HCC samples in TCGA database, and was confirmed to be elevated in HCC cell lines. Functionally, LINC00467 depletion impeded proliferation and invasion, induced apoptosis, and promoted cellular sensitivity to Axitinib in HCC. Mechanistically, LINC00467 performed as a sponge of microRNA (miR)-509-3p and upregulated the expression of platelet-derived growth factor receptor alpha (PDGFRA) in HCC cells. In conclusion, our study illustrated that LINC00467 promoted proliferation and invasion, impedes apoptosis, and contributed to Axitinib resistance of hepatocellular carcinoma through miR-509-3p/PDGFRA, indicating LINC00467 as a promising biological target for HCC treatment.

MeSH terms

  • Axitinib* / therapeutic use
  • Carcinoma, Hepatocellular* / drug therapy
  • Carcinoma, Hepatocellular* / genetics
  • Carcinoma, Hepatocellular* / pathology
  • Cell Line, Tumor
  • Cell Movement
  • Cell Proliferation
  • Gene Expression Regulation, Neoplastic
  • Gene Knockdown Techniques
  • Humans
  • Liver Neoplasms* / drug therapy
  • Liver Neoplasms* / genetics
  • Liver Neoplasms* / metabolism
  • MicroRNAs* / genetics
  • MicroRNAs* / metabolism
  • RNA, Long Noncoding / genetics*
  • Receptor, Platelet-Derived Growth Factor alpha / genetics

Substances

  • MIRN509 microRNA, human
  • MicroRNAs
  • RNA, Long Noncoding
  • Axitinib
  • Receptor, Platelet-Derived Growth Factor alpha