关键词: DNA methylation KCTD8 PI3K/AKT signaling pathway hepatocellular carcinoma tumor suppressor

Mesh : Humans Carcinoma, Hepatocellular / genetics pathology metabolism Liver Neoplasms / genetics pathology metabolism Proto-Oncogene Proteins c-akt / metabolism Phosphatidylinositol 3-Kinases / metabolism Animals DNA Methylation Epigenesis, Genetic Signal Transduction Mice Cell Line, Tumor Female Male Gene Expression Regulation, Neoplastic Gene Silencing Cell Proliferation Middle Aged Mice, Nude Prognosis

来  源:   DOI:10.1080/17501911.2024.2370590   PDF(Pubmed)

Abstract:
Aim: The aim of current study is to explore the epigenetic changes and function of KCTD8 in human hepatocellular carcinoma (HCC). Materials & methods: HCC cell lines and tissue samples were employed. Methylation specific PCR, flow cytometry, immunoprecipitation and xenograft mouse models were used.Results: KCTD8 was methylated in 44.83% (104/232) of HCC and its methylation may act as an independent poor prognostic marker. KCTD8 expression was regulated by DNA methylation. KCTD8 suppressed HCC cell growth both in vitro and in vivo via inhibiting PI3K/AKT pathway.Conclusion: Methylation of KCTD8 is an independent poor prognostic marker, and epigenetic silencing of KCTD8 increases the malignant tendency in HCC.
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摘要:
目的:本研究的目的是探讨KCTD8在人肝细胞癌(HCC)中的表观遗传学变化和功能。材料和方法:采用HCC细胞系和组织样品。甲基化特异性PCR,流式细胞术,使用免疫沉淀和异种移植小鼠模型。结果:KCTD8在44.83%(104/232)的HCC中甲基化,其甲基化可能是一个独立的不良预后标志物。KCTD8表达受DNA甲基化调控。KCTD8通过抑制PI3K/AKT途径在体外和体内抑制HCC细胞生长。结论:KCTD8甲基化是一个独立的预后不良指标。KCTD8的表观遗传沉默增加了HCC的恶性倾向。
[方框:见正文]。
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