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Loss of phospholipase Cγ1 suppresses hepatocellular carcinogenesis through blockade of STAT3-mediated cancer development

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Author(s)
Eun-Bi SeoHyun-Jun JangSun-Ho KwonYong-Jin KwonSeul-Ki KimSong-Hee LeeAe Jin JeongHyun Mu ShinYong-Nyun KimStephanie MaHaeryoung KimYun-Han LeePann-Ghill SuhSang-Kyu Ye
Keimyung Author(s)
Lee, Yun Han
Department
Dept. of Molecular Medicine (분자의학)
Journal Title
Hepatol Commun
Issued Date
2022
Volume
6
Issue
11
Abstract
Phospholipase C gamma 1 (PLCγ1) plays an oncogenic role in several cancers, alongside its usual physiological roles. Despite studies aimed at identifying the effect of PLCγ1 on tumors, the pathogenic role of PLCγ1 in the tumorigenesis and development of hepatocellular carcinoma (HCC) remains unknown. To investigate the function of PLCγ1 in HCC, we generated hepatocyte-specific PLCγ1 conditional knockout (PLCγ1f/f; Alb-Cre) mice and induced HCC with diethylnitrosamine (DEN). Here, we identified that hepatocyte-specific PLCγ1 deletion effectively prevented DEN-induced HCC in mice. PLCγ1f/f; Alb-Cre mice showed reduced tumor burden and tumor progression, as well as a decreased incidence of HCC and less marked proliferative and inflammatory responses. We also showed that oncogenic phenotypes such as repressed apoptosis, and promoted proliferation, cell cycle progression and migration, were induced by PLCγ1. In terms of molecular mechanism, PLCγ1 regulated the activation of signal transducer and activator of transcription 3 (STAT3) signaling. Moreover, PLCγ1 expression is elevated in human HCC and correlates with a poor prognosis in patients with HCC. Our results suggest that PLCγ1 promotes the pathogenic progression of HCC, and PLCγ1/STAT3 axis was identified as a potential therapeutic target pathway for HCC.
Keimyung Author(s)(Kor)
이윤한
Publisher
School of Medicine (의과대학)
Type
Article
ISSN
2471-254X
Source
https://aasldpubs.onlinelibrary.wiley.com/doi/10.1002/hep4.2077
DOI
10.1002/hep4.2077
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/44536
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Molecular Medicine (분자의학)
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