Long noncoding RNA DDX11-AS1 represses sorafenib-induced ferroptosis in hepatocellular carcinoma cells via Nrf2-Keap1

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Liang Wang1, Liming Wang2

  • 1The Second Affiliated Hospital of Dalian Medical University, Dalian, China, NO. 467, Zhongshan Road, Shahekou district, Liaoning, 116000. liangsurgery@163.com.

Discover Oncology
|October 10, 2024
PubMed

Insights

The oncogene DDX11-AS1 promotes sorafenib resistance in hepatocellular carcinoma (HCC) by blocking ferroptosis. This occurs through activating the Nrf2-Keap1 pathway, offering a potential strategy to improve HCC treatment.

Area of Science:

  • Molecular Oncology
  • Hepatocellular Carcinoma Research
  • Drug Resistance Mechanisms

Background:

  • Sorafenib is a primary treatment for advanced hepatocellular carcinoma (HCC).
  • Emerging resistance to sorafenib significantly limits its therapeutic efficacy.
  • The oncogene DDX11 antisense RNA 1 (DDX11-AS1) is implicated in various cancers, but its role in sorafenib resistance in HCC is uncharacterized.

Purpose of the Study:

  • To investigate the role of DDX11-AS1 in sorafenib resistance in HCC.
  • To elucidate the underlying molecular mechanisms by which DDX11-AS1 influences sorafenib resistance.

Main Methods:

  • Analysis of DDX11-AS1 expression in sorafenib-resistant HCC cells.
  • Investigation of DDX11-AS1's effect on ferroptosis.
  • Elucidation of DDX11-AS1's interaction with the Nrf2-Keap1 pathway.

Main Results:

  • DDX11-AS1 expression is upregulated in sorafenib-resistant HCC cells.
  • DDX11-AS1 suppresses sorafenib-induced ferroptosis, contributing to resistance.
  • DDX11-AS1 activates the Nrf2-Keap1 pathway by enhancing Nrf2 stability and nuclear translocation.

Conclusions:

  • DDX11-AS1 promotes sorafenib resistance in HCC by inhibiting ferroptosis via the Nrf2-Keap1 pathway.
  • Targeting DDX11-AS1 presents a potential therapeutic strategy to overcome sorafenib resistance in HCC.
Keywords:
FerroptosisNrf2; Keap1Sorafenib

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