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Downregulation of MTHFD2 Inhibits Proliferation and Enhances Chemosensitivity in Hepatocellular Carcinoma via

Jie Wang1, Ze Yu1, Yixiao Jiang2

  • 1Cellular and Molecular Biology Laboratory, Zhoushan Hospital, Wenzhou Medical University, 316021 Zhoushan, Zhejiang, China.

Frontiers in Bioscience (Landmark Edition)
|January 30, 2024
PubMed
Abstract

Insights

Methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) is upregulated in hepatocellular carcinoma (HCC), driving proliferation and reducing drug sensitivity. Targeting MTHFD2 may improve HCC therapy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) is implicated in cancer progression.
  • Its specific role in hepatocellular carcinoma (HCC) cell proliferation and chemosensitivity is not well understood.

Purpose of the Study:

  • To investigate the role of MTHFD2 in HCC cell proliferation and chemosensitivity.
  • To explore MTHFD2 as a potential therapeutic target for HCC.

Main Methods:

  • Immunohistochemistry and qRT-PCR to assess MTHFD2 expression in 95 HCC tissues.
  • Bioinformatics analyses (GSEA, KEGG) to predict involved signaling pathways.
  • MTHFD2 knockdown experiments using CCK-8 and EdU assays to evaluate anti-tumor effects and drug sensitivity.

Main Results:

  • MTHFD2 was frequently upregulated in HCC tissues, correlating with poor prognosis when co-expressed with Ki67.
  • MTHFD2 knockdown inhibited HCC cell proliferation and enhanced sensitivity to sorafenib and lenvatinib.
  • The PI3K/AKT pathway was identified as a key mediator of MTHFD2's effects on proliferation and chemosensitivity.

Conclusions:

  • MTHFD2 significantly influences HCC cell proliferation and chemosensitivity.
  • MTHFD2 represents a promising novel pharmacological target for enhancing hepatocellular carcinoma treatment strategies.
Keywords:
HCCKi-67MTHFD2chemosensitivityproliferation

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