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Updated: Sep 2, 2025

An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis
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CircFMN2 Boosts Sorafenib Resistance in Hepatocellular Carcinoma Cells via Upregulating CNBP by Restraining

Chen Fan1, Xiaoli Zhu2, Qi Zhou1

  • 1Department of Intervention, Wuxi People's Hospital, Nanjing Medical University, Wuxi 214023, China.

Journal of Oncology
|August 1, 2022
PubMed
Abstract

Insights

Newly discovered circFMN2 RNA is highly expressed in sorafenib-resistant hepatocellular carcinoma (HCC) cells. It promotes HCC cell proliferation and drug resistance by upregulating CNBP, offering a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Noncoding RNAs play crucial roles in hepatocellular carcinoma (HCC) development.
  • circFMN2, a novel functional RNA, has been identified in other cancers but its role in HCC remains unexplored.

Purpose of the Study:

  • To investigate the role of circFMN2 in sorafenib-resistant HCC cells.
  • To elucidate the underlying mechanism of circFMN2 in promoting sorafenib resistance.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) to assess circFMN2 levels.
  • Cell proliferation, apoptosis assays, and Western blot to analyze cellular changes and protein levels.
  • RNA pull-down and immunoprecipitation assays to determine circFMN2-CNBP interaction.

Main Results:

  • CircFMN2 expression was significantly higher in multidrug-resistant (MDR) HCC cells.
  • CircFMN2 overexpression enhanced proliferation and sorafenib resistance, while depletion had the opposite effect.
  • CircFMN2 directly binds to CNBP, upregulating its levels by inhibiting ubiquitination, thereby promoting sorafenib resistance.

Conclusions:

  • CircFMN2 is aberrantly expressed in sorafenib-resistant HCC.
  • CircFMN2 contributes to sorafenib resistance by upregulating CNBP through the inhibition of ubiquitination.

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