Has_circ_0008583 modulates hepatocellular carcinoma progression through the miR-1301-3p/METTL3 pathway

Bioengineered. 2022 Jan;13(1):1185-1197. doi: 10.1080/21655979.2021.2017579.

Abstract

Has_circ_0008583 is reported to be involved in the progression of hepatocellular carcinoma (HCC), while its biological role in HCC remains unclear. Here, the qRT-PCR was used to detect the expression of has_circ_0008583. The CCK-8 kit was performed to measure cell proliferation. The cell migration and invasion were evaluated by Transwell. A dual-luciferase reporter assay was performed to confirm the target combination between the genes in has_circ_0008583/miR-1301-3p/METTL3 axis. The in vivo role of has_circ_0008583 was verified by murine xenograft assay. Our data showed that hsa_circ_0008583 was upregulated in HCC tissues and cells. Hsa_circ_0008583 overexpression promoted Hep3B cell proliferation, migration and invasion, but hsa_circ_0008583 silencing had an opposing influence. MiR-1301-3p is directly bound to hsa_circ_0008583 and METTL3. MiR-1301-3p overexpression or METTL3 knockdown could partially counteract hsa_circ_0008583 overexpression-mediated influence on HCC cell behaviors. In addition, hsa_circ_0008583 depletion inhibits HCC tumor growth in vivo. In conclusion, hsa_circ_0008583 promotes HCC progression through the miR-1301-3p/METTL3 axis.

Keywords: Has_circ_0008583; Hepatocellular carcinoma; METTL3; miR-1301-3p.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Carcinoma, Hepatocellular* / genetics
  • Carcinoma, Hepatocellular* / pathology
  • Cell Line, Tumor
  • Cell Proliferation / genetics
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Liver Neoplasms* / genetics
  • Liver Neoplasms* / pathology
  • Methyltransferases / metabolism
  • Mice
  • MicroRNAs* / genetics
  • MicroRNAs* / metabolism
  • RNA, Circular / genetics

Substances

  • MIRN1301 microRNA, human
  • MicroRNAs
  • RNA, Circular
  • Methyltransferases
  • Mettl3 protein, mouse
  • METTL3 protein, human

Grants and funding

This work was supported by Natural Science Foundation of Jiangxi, China (Grant Number 20202BABL206018); the National Natural Science Foundation of China (Grant number 81960440 and 82070594) and the Financial Support Program for Academic Leaders of Major Disciplines in Jiangxi Province, China (Grant number 20182BCB22018).