Regulation of microRNA miR-197-3p/CDC28 protein kinase regulatory subunit 1B (CKS1B) axis by Circular RNA hsa_circ_0000285 promotes glioma progression

Bioengineered. 2022 Mar;13(3):4757-4772. doi: 10.1080/21655979.2022.2031673.

Abstract

Circular RNA circ_0000285 is differentially expressed in several malignancies; however, its role in gliomas is under investigation. Reverse transcription quantitative polymerase chain reaction was conducted to evaluate the expression of circ_0000285, miR-197-3p, and CDC28 protein kinase regulatory subunit 1B (CKS1B) in glioma tissues and cells. Cell Counting Kit-8 and Transwell invasion assays coupled with Western blotting analysis using anti-Bax and anti-Bcl-2 antibodies were performed to evaluate cell proliferation, invasion, and apoptosis. Luciferase reporter and AGO2 RNA immunoprecipitation assays were conducted to verify the interaction between miR-197-3p and circ_0000285 or CKS1B. Xenograft tumor growth was evaluated in mice. We noted that circ_0000285 was highly expressed in glioma tissues and cells and that circ_0000285-silencing retarded tumor growth both in vitro and in vivo. This effect was mediated by the binding of circ_0000285 to miR-197-3p, which silenced CKS1B, an essential driver of glioma cell proliferation and invasion. Thus, circ_0000285 boosted glioma progression by regulating the miR-197-3p/CKS1B axis, highlighting a novel competing endogenous RNA circuit of glioma progression.

Keywords: ceRNA; circRNA; glioma; miRNA.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • CDC2-CDC28 Kinases* / genetics
  • Cell Line, Tumor
  • Cell Movement / genetics
  • Cell Proliferation / genetics
  • Gene Expression Regulation, Neoplastic
  • Glioma* / metabolism
  • Humans
  • Mice
  • MicroRNAs* / genetics
  • RNA, Circular* / genetics

Substances

  • CKS1B protein, human
  • MIRN197 microRNA, human
  • MicroRNAs
  • RNA, Circular
  • CDC2-CDC28 Kinases

Grants and funding

This work was supported by Hubei Provincial Health Commission Project (2019-2020) ‘Interleukin-33 Blocking Effect and Mechanism of Tumor Immune Escape’ (WJ2019M099)