TRIM24 通过 AMPK 信号促进肝癌进展。
TRIM24 promotes hepatocellular carcinoma progression via AMPK signaling.
机构信息
Department of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital of Wenzhou Medical University, 325000, Wenzhou, China.
Laboratory of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital of Wenzhou Medical University, 325000, Wenzhou, China.
出版信息
Exp Cell Res. 2018 Jun 15;367(2):274-281. doi: 10.1016/j.yexcr.2018.04.006. Epub 2018 Apr 6.
Hepatocellular carcinoma (HCC) is one of the most common cancers diagnosed worldwide. However, the mechanism underlying HCC pathogenesis remains unknown. In the present study, TRIM24 was found increased in human HCC clinical samples and positively correlated with HCC tumor grade. Furthermore, TRIM24 knockdown inhibits proliferation and migration in a human HCC cell line in vitro while also inhibiting tumor growth in vivo. Mechanistically, TRIM24 appears to promote liver tumor development via AMPK signaling as AMPK knockdown alleviated the in vitro and in vivo effects of TRIM24 knockdown in a human HCC cell line. Taken together, these data enhance our understanding of HCC development in addition to highlighting TRIM24-regulated AMPK signaling as a potential therapeutic target for HCC treatment.
肝细胞癌 (HCC) 是全球最常见的癌症之一。然而，HCC 发病机制的具体机制尚不清楚。在本研究中，发现 TRIM24 在人 HCC 临床样本中增加，并与 HCC 肿瘤分级呈正相关。此外，TRIM24 敲低抑制体外人 HCC 细胞系的增殖和迁移，同时也抑制体内肿瘤生长。从机制上讲，TRIM24 似乎通过 AMPK 信号促进肝肿瘤的发展，因为 AMPK 敲低减轻了人 HCC 细胞系中 TRIM24 敲低的体外和体内作用。综上所述，这些数据除了强调 TRIM24 调节的 AMPK 信号作为 HCC 治疗的潜在治疗靶点外，还增进了我们对 HCC 发展的理解。
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