Du, LiLiDuJi, YichunYichunJiXin, BingBingXinZhang, JiemengJiemengZhangLI-CHUN LUGlass, Christopher KChristopher KGlassFeng, Gen-ShengGen-ShengFeng2023-05-092023-05-092023-02-232352345Xhttps://scholars.lib.ntu.edu.tw/handle/123456789/630920Complex communications between hepatocytes and Kupffer cells (KCs) are known to drive or suppress hepatocarcinogenesis, with controversial data in the literature. In previous experiments that aimed to decipher hepatocyte/KC interactions, we unexpectedly unveiled a tumor-suppressing effect of polyinosinic-polycytidylic acid, a widely used inducer of MX dynamin like GTPase 1 (Mx1)-cre expression, which questioned a theory of interleukin 1a/6 cytokine circuit in hepatocyte/KC communication. The goal of this study was to clarify the controversy and decipher unique functions of KCs and non-KC macrophages in liver tumorigenesis.enHepatocarcinogenesis; Hepatocyte/Kupffer Cell Communication; Tumor Microenvironment; Tumor-Associated MacrophagesShp2 Deficiency in Kupffer Cells and Hepatocytes Aggravates Hepatocarcinogenesis by Recruiting Non-Kupffer Macrophagesjournal article10.1016/j.jcmgh.2023.02.011368282812-s2.0-85152946993https://api.elsevier.com/content/abstract/scopus_id/85152946993