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MEK1 promotes YAP and their interaction is critical for tumorigenesis in liver cancer
Author(s) -
Li Lanlan,
Wang Jiayi,
Zhang Yue,
Zhang Yan,
Ma Lifang,
Weng Wenhao,
Qiao Yongxia,
Xiao Weifan,
Wang Hongmei,
Yu Wenjun,
Pan Qiuhui,
He Yunyan,
Sun Fenyong
Publication year - 2013
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2013.10.042
Subject(s) - hippo signaling pathway , ubiquitin ligase , microbiology and biotechnology , effector , protein kinase a , carcinogenesis , kinase , biology , cancer research , ubiquitin , cancer , chemistry , biochemistry , genetics , gene
Mitogen‐activated protein kinase kinase 1 (MAP2K1/MEK1) as well as Yes‐associated protein (YAP), the downstream effector of Hippo signaling pathway, is linked to hepatocarcinogenesis. However, little is known about whether and how MEK1 interacts with YAP. In this study, we find that MEK1‐YAP interaction is critical for liver cancer cell proliferation and maintenance of transformed phenotypes both in vitro and in vivo. Moreover, MEK1 and YAP proteins are closely correlated in human liver cancer samples. Mechanistically, inhibition of MEK1 by both PD98059 and U0126 as well as RNAi reduces beta‐transducin repeat containing E3 ubiquitin protein ligase (BTRC), which acts as a potential endogenous YAP protector.