2. Academic Validation
  3. Loss of FAM172A gene prompts cell proliferation in liver regeneration

Loss of FAM172A gene prompts cell proliferation in liver regeneration

  • Mol Cell Biochem. 2025 Feb;480(2):1183-1195. doi: 10.1007/s11010-024-05044-7.
Herui Wei # 1,  Yifan Zhang # 2 3,  Meixin Gao 4,  Junru Yang 1,  Shiwei Wang 2 3,  Xingang Zhou 5,  Hongshan Wei 6,  Fan Xiao 7 8 9 10
Affiliations

Affiliations

  • 1 Department of Gastroenterology, Beijing Ditan Hospital, Capital Medical University, Beijing, 100015, China.
  • 2 Department of Gastroenterology, Peking University People's Hospital, Beijing, 100044, China.
  • 3 Clinical Center of Immune-Mediated Digestive Diseases, Peking University People's Hospital, Beijing, 100044, China.
  • 4 Department of Gastroenterology, Beijing Tongren Hospital, Capital Medical University, Beijing, 100176, China.
  • 5 Department of Pathology, Beijing Ditan Hospital, Capital Medical University, Beijing, 100015, China.
  • 6 Department of Gastroenterology, Beijing Ditan Hospital, Capital Medical University, Beijing, 100015, China. [email protected].
  • 7 Beijing Key Laboratory of Emerging Infectious Diseases, Institute of Infectious Diseases, Beijing Ditan Hospital, Capital Medical University, Beijing, 100015, China. [email protected].
  • 8 Beijing Institute of Infectious Diseases, Beijing, 100015, China. [email protected].
  • 9 National Center for Infectious Diseases, Beijing Ditan Hospital, Capital Medical University, Beijing, 100015, China. [email protected].
  • 10 National Key Laboratory of Intelligent Tracking and Forecasting for Infectious Diseases, Beijing Ditan Hospital, Capital Medical University, Beijing, 100015, China. [email protected].
  • # Contributed equally.
PMID: 38896202 DOI: 10.1007/s11010-024-05044-7
Abstract

The present study was designed to explore the function of FAM172A in liver regeneration and HCC. Mice were sacrificed after 70% partial hepatectomy (PH). RNA Sequencing was performed on primary hepatocytes of WT and FAM172A-/- mice. We used HepG2 cells to construct cell lines with stably knockdown and overexpression of FAM172A. The expression of FAM172A in liver tissues was investigated by immunohistochemical staining, and we also used public database to perform survival analysis and prognostic model in HCC. Compared with WT mice after PH, normalized liver weight/body weight (LW/BW) ratio and the proliferating cell nuclear antigen (PCNA) protein level of FAM172A-/- mice elevated. The DEGs were mainly enriched in inflammatory response, tumor necrosis factor production, and wound healing. FAM172A knockdown enhanced the NFκB-TNFα and pERK-YAP1-Cyclin D1 axis. FAM172A peptide inhibited proliferation of primary hepatocytes. Moreover, the low expression of FAM172A in human HCC tissues implies a lower likelihood of survival and a valid diagnostic marker for HCC. Loss of FAM172A gene promotes cell proliferation by pERK-YAP1-Cyclin D1 and pNFκB-TNFα pathways during liver regeneration after PH. FAM172A may be a favorable diagnosis marker of HCC.

Keywords

FAM172A; Cell proliferation; Hepatocellular carcinoma; Liver regeneration; Partial hepatectomy.

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