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Identification of RUNX3 as a component of the MST/Hpo signaling pathway

机译:鉴定RUNX3作为msT / Hpo信号传导途径的组分

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摘要

Recent genetic screens of fly mutants and molecular analysis have revealed that the Hippo (Hpo) pathway controls both cell proliferation and cell death. Deregulation of its human counterpart (the MST pathway) has been implicated in human cancers. However, how this pathway is linked with the known tumor suppressor network remains to be established. RUNX3 functions as a tumor suppressor of gastric cancer, lung cancer, bladder cancer, and colon cancer. Here, we show that RUNX3 is a principal and evolutionarily conserved component of the MST pathway. SAV1/WW45 facilitates the close association between MST2 and RUNX3. MST2, in turn, stimulates the SAV1-RUNX3 interaction. In addition, we show that siRNA-mediated RUNX3 knockdown abolishes MST/Hpo-mediated cell death. By establishing that RUNX3 is an endpoint effector of the MST pathway and that RUNX3 is capable of inducing cell death in cooperation with MST and SAV1, we define an evolutionarily conserved novel regulatory mechanism loop for tumor suppression in human cancers.
机译:蝇蝇突变体的最新遗传学筛查和分子分析显示,河马(Hpo)途径既控制细胞增殖,又控制细胞死亡。人类癌症中已牵涉到其人类对应物(MST途径)的失控。然而,该途径如何与已知的肿瘤抑制网络联系尚待确定。 RUNX3用作胃癌,肺癌,膀胱癌和结肠癌的肿瘤抑制因子。在这里,我们表明RUNX3是MST途径的主要组成部分,并且在进化上是保守的。 SAV1 / WW45有助于MST2和RUNX3之间的紧密关联。 MST2反过来刺激SAV1-RUNX3交互。此外,我们显示,siRNA介导的RUNX3敲除消除了MST / Hpo介导的细胞死亡。通过确定RUNX3是MST途径的终点效应子,并且RUNX3能够与MST和SAV1协同诱导细胞死亡,我们定义了人类肿瘤中肿瘤抑制的进化保守的新型调控机制环。

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