2. Academic Validation
  3. Epigenetic silencing of KCTD8 promotes hepatocellular carcinoma growth by activating PI3K/AKT signaling

Epigenetic silencing of KCTD8 promotes hepatocellular carcinoma growth by activating PI3K/AKT signaling

  • Epigenomics. 2024;16(13):929-944. doi: 10.1080/17501911.2024.2370590.
Jing Zhou 1 2,  Meiying Zhang 2,  Aiai Gao 2,  James G Herman 3,  Mingzhou Guo 1 2 4
Affiliations

Affiliations

  • 1 School of Medicine, NanKai University, Tianjin, 300071, China.
  • 2 Department of Gastroenterology & Hepatology, the First Medical Center, Chinese PLA General Hospital, Beijing, 100853, China.
  • 3 The Hillman Cancer Center, University of Pittsburgh Cancer Institute, Pittsburgh, PA 15213, USA.
  • 4 National Key Laboratory of Kidney Diseases, Beijing, 100853, China.
PMID: 39023358 DOI: 10.1080/17501911.2024.2370590
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.

Keywords

DNA methylation; KCTD8; PI3K/AKT signaling pathway; hepatocellular carcinoma; tumor suppressor.

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