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MEK1 promotes YAP and their interaction is critical for tumorigenesis in liver cancer

Lanlan Li1, Jiayi Wang, Yue Zhang

  • 1Department of Clinical Laboratory Medicine, Shanghai Tenth People's Hospital of Tongji University, Shanghai 200072, China; Department of Laboratory Medicine, Chongqing Zhongshan Hospital, Chongqing 400013, China.

FEBS Letters
|November 12, 2013
PubMed

Insights

Mitogen-activated protein kinase kinase 1 (MAP2K1/MEK1) interaction with Yes-associated protein (YAP) drives liver cancer cell growth. MEK1 inhibition reduces BTRC, a YAP protector, impacting cancer progression.

Area of Science:

  • Molecular oncology
  • Cell signaling pathways

Background:

  • Mitogen-activated protein kinase kinase 1 (MAP2K1/MEK1) and Yes-associated protein (YAP) are implicated in hepatocarcinogenesis.
  • The mechanistic link between MEK1 and YAP in liver cancer remains largely unexplored.

Purpose of the Study:

  • To investigate the interaction between MEK1 and YAP in liver cancer.
  • To elucidate the functional significance of MEK1-YAP interplay in hepatocarcinogenesis.

Main Methods:

  • Utilized chemical inhibitors (PD98059, U0126) and RNA interference (RNAi) to inhibit MEK1.
  • Assessed liver cancer cell proliferation and transformed phenotypes in vitro and in vivo.
  • Analyzed protein correlation in human liver cancer samples.
  • Investigated the effect of MEK1 inhibition on beta-transducin repeat containing E3 ubiquitin protein ligase (BTRC) expression.

Main Results:

  • MEK1-YAP interaction is crucial for liver cancer cell proliferation and maintaining transformed phenotypes.
  • MEK1 and YAP proteins show a close correlation in human liver cancer tissues.
  • MEK1 inhibition leads to reduced levels of BTRC, identified as a potential YAP protector.

Conclusions:

  • The MEK1-YAP axis plays a critical role in liver cancer progression.
  • Targeting MEK1 may represent a therapeutic strategy by affecting YAP stability via BTRC modulation.
Keywords:
3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromideBTRCCell signalingERK1/2HCCHippo pathwayIFIHCMTTTMAhepatocellular carcinomaimmunofluorescenceimmunohistochemistrytissue microarray analysis

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