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Loss of FAM172A gene prompts cell proliferation in liver regeneration

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机构： [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]Beijing Key Laboratory of Emerging Infectious Diseases, Institute of Infectious Diseases, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China [7]Beijing Institute of Infectious Diseases, Beijing 100015, China [8]National Center for Infectious Diseases, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China [9]National Key Laboratory of Intelligent Tracking and Forecasting for Infectious Diseases, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China

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关键词： FAM172A Liver regeneration Partial hepatectomy Cell proliferation Hepatocellular carcinoma

摘要：

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.© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

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出版当年[2025]版：

大类 | 3 区生物学

小类 | 3 区细胞生物学

最新[2025]版：

大类 | 3 区生物学

小类 | 3 区细胞生物学

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出版当年[2023]版：

Q3 CELL BIOLOGY

最新[2023]版：

Q3 CELL BIOLOGY

影响因子： 3.5 最新[2023版] 3.3 最新五年平均 3.5 出版当年[2023版] 3.3 出版当年五年平均 4.3 出版前一年[2022版]

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第一作者机构： [1]Department of Gastroenterology, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China

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通讯机构： [6]Beijing Key Laboratory of Emerging Infectious Diseases, Institute of Infectious Diseases, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China [7]Beijing Institute of Infectious Diseases, Beijing 100015, China [8]National Center for Infectious Diseases, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China [9]National Key Laboratory of Intelligent Tracking and Forecasting for Infectious Diseases, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China

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Loss of FAM172A gene prompts cell proliferation in liver regeneration

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