咖啡因
MAPK/ERK通路
激酶
癌症研究
细胞生长
信号转导
细胞生物学
化学
MEK抑制剂
表皮生长因子受体
细胞凋亡
药理学
生物
受体
内分泌学
生物化学
作者
Jun‐ichi Okano,Takakazu Nagahara,Kazuya Matsumoto,Yoshikazu Murawaki
标识
DOI:10.1111/j.1742-7843.2008.00231.x
摘要
Abstract: Caffeine has been reported to prevent hepatocarcinogenesis. We investigated the molecular mechanisms by which caffeine inhibits the growth of hepatocellular carcinoma (HCC) cells. We found that caffeine inhibited the proliferation of HCC cells via cell cycle arrest independent of apoptosis. We revealed a novel signalling axis for caffeine involving activation of the mitogen‐activated ERK‐regulating kinase (MEK)/extracellular signal‐regulated kinase (ERK) pathway that resulted in the downstream up‐regulation of epidermal growth factor receptor (EGFR), although the MEK/ERK/EGFR signalling pathway was not involved in the growth inhibitory effect of caffeine. Our data reveal that caffeine could be a promising candidate for the treatment of patients with HCC.
科研通智能强力驱动
Strongly Powered by AbleSci AI