Downregulation of SETD5 suppresses the tumorigenicity of hepatocellular carcinoma cells

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Downregulation of SETD5 suppresses the tumorigenicity of hepatocellular carcinoma cells
Mijin Park; Byul Moon; Jong-Hwan Kim; Seung-Jin Park; Seon-Kyu Kim; K Park; J Kim; Seon-Young KimJeong Hoon KimJung Ae Kim
Bibliographic Citation
Molecules and Cells, vol. 45, no. 8, pp. 550-563
Publication Year
Hepatocellular carcinoma (HCC) is an aggressive and incurable cancer. Although understanding of the molecular pathogenesis of HCC has greatly advanced, therapeutic options for the disease remain limited. In this study, we demonstrated that SETD5 expression is positively associated with poor prognosis of HCC and that SETD5 depletion decreased HCC cell proliferation and invasion while inducing cell death. Transcriptome analysis revealed that SETD5 loss downregulated the interferon-mediated inflammatory response in HCC cells. In addition, SETD5 depletion downregulated the expression of a critical glycolysis gene, PKM (pyruvate kinase M1/2), and decreased glycolysis activity in HCC cells. Finally, SETD5 knockdown inhibited tumor growth in xenograft mouse models. These results collectively suggest that SETD5 is involved in the tumorigenic features of HCC cells and that targeting SETD5 may suppress HCC progression.
EpigeneticsGlycolysisHepatocellular carcinomaHistone lysine methyltransferaseInterferon responseSETD5
Korea Soc-Assoc-Inst
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Aging Convergence Research Center > 1. Journal Articles
Division of Biomedical Research > Disease Target Structure Research Center > 1. Journal Articles
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