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  • Title: New tumor suppressor CXXC finger protein 4 inactivates mitogen activated protein kinase signaling.
    Author: Lu H, Jin W, Sun J, Feng L, Lan H, Shen Q, Ma Y, Li J, Yue Y, Jin H, Wang X.
    Journal: FEBS Lett; 2014 Sep 17; 588(18):3322-6. PubMed ID: 25064842.
    Abstract:
    As a well-characterized master player in epigenetic regulatory network, EZH2 is widely implicated in the development of many malignancies. We previously found that EZH2 promoted Wnt/β-catenin activation through downregulation of CXXC4 expression. In this report, we demonstrated that CXXC4 inhibited MAPK signaling through binding to ERK-1/2 and abrogating the interaction of ERK 1/2 with MEK1/2. L183, the critical residue in CXXC4 ERK D domain, was found to be essential for CXXC4-ERK 1/2 interaction and the growth inhibitory effect of CXXC4 in human cancer cells. In summary, CXXC4 directly disrupted MEK1/2-ERK 1/2 interaction to inactivate MAPK signaling. L183 site is indispensable for the binding of CXXC4 to ERK1/2 and growth inhibitory effect of CXXC4. Therefore, EZH2 can activate MAPK signaling by inhibiting CXXC4 expression.
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