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Identification of differentially expressed mRNA/lncRNA modules in acutely regorafenib-treated sorafenib-resistant

Mina Baek1, Minjae Kim1, Hae In Choi1

  • 1Department of Molecular and Life Science, Hanyang University, Ansan, Republic of Korea.

Plos One
|April 11, 2024
PubMed

Insights

Regorafenib shows promise as a second-line treatment for advanced hepatocellular carcinoma (HCC) in patients resistant to sorafenib. This study identified key molecular pathways and long non-coding RNAs involved in the response to regorafenib.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Sorafenib is a standard first-line treatment for advanced hepatocellular carcinoma (HCC).
  • Acquired resistance to sorafenib (SR) is a significant clinical challenge in HCC management.
  • Identifying effective second-line therapies is crucial for improving patient outcomes.

Purpose of the Study:

  • To investigate the efficacy of regorafenib (Rego) as a second-line treatment for sorafenib-resistant (SR) HCC cells.
  • To explore the molecular mechanisms and signaling pathways affected by regorafenib treatment in SR HCC.
  • To identify potential long non-coding RNA (lncRNA) biomarkers associated with regorafenib response.

Main Methods:

  • Generation of sorafenib-resistant (SR) HCC cell models.
  • Analysis of affected signaling pathways, including PI3K-Akt, TNF, cAMP, and TGF-beta.
  • Assessment of gene expression changes related to nucleosome assembly and epigenetic regulation.
  • Weighted gene co-expression network analysis (WGCNA) to identify differentially expressed lncRNA (DElncRNA) modules.
  • Identification and association of DElncRNAs with differentially expressed mRNAs (DEmRNAs) to form co-expression modules.

Main Results:

  • Regorafenib treatment reversed TGF-beta signaling gene expression but upregulated PI3K-Akt signaling genes in SR HCC cells.
  • Regorafenib modulated gene expression involved in nucleosome assembly and epigenetic regulation.
  • WGCNA identified four DElncRNA modules significantly associated with regorafenib efficacy in SR cells.
  • Eleven putative DElncRNAs were identified and linked with DEmRNAs, forming co-expression modules.

Conclusions:

  • Regorafenib demonstrates potential as a second-line therapy for SR HCC by modulating specific signaling pathways and epigenetic mechanisms.
  • Identified DElncRNA/DEmRNA co-expression modules offer insights into the molecular underpinnings of regorafenib response.
  • These findings provide a foundation for further research into regorafenib's therapeutic potential and biomarker discovery in resistant HCC.

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