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miR-133 is a key negative regulator of CDC42-PAK pathway in gastric cancer

机译：miR-133是CDC42-PAK途径在胃癌中的关键负调控因子

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摘要

Cell division cycle 42 (CDC42), an important member of the Ras homolog (Rho) family, plays a key role in regulating multiple cellular processes such as cell cycle progression, migration, cell cytoskeleton organization, cell fate determination and differentiation. Among the downstream effectors of CDC42, P21-activated kinases (PAKs) obtain the most attention. Although a large body of evidence indicates that CDC42/PAKs pathway plays important role in tumor growth, invasion and metastasis, the mechanism of their negative regulation remains unclear. Here, we identified CDC42, a PAKs activating factor, was a target of miR-133. Ectopic overexpression of miRNAs not only downregulated CDC42 expression and PAKs activation, but also inhibited cancer cell proliferation and migration. We also found that miR-133 was down-regulated in 180 pairs gastric cancer tissues. miR-133 expression was negatively associated with tumor size, invasion depth and peripheral organmetastasis. Besides, dysfunction of miR-133 was an independent prognosis factor for overall survival. Our findings could provide newinsights into themolecular mechanisms of gastric carcinogenesis, andmay help facilitating development of CDC42/PAK-based therapies for human cancer.
机译：细胞分裂周期42（CDC42）是Ras同源物（Rho）家族的重要成员，在调节多个细胞过程（例如细胞周期进程，迁移，细胞骨架组织，细胞命运确定和分化）中起着关键作用。在CDC42的下游效应子中，P21激活的激酶（PAK）获得了最多的关注。尽管大量证据表明CDC42 / PAKs途径在肿瘤生长，侵袭和转移中起重要作用，但其负调控的机制仍不清楚。在这里，我们确定了CDC42，一种PAKs激活因子，是miR-133的靶标。 miRNA的异位过表达不仅下调CDC42表达和PAKs激活，而且抑制癌细胞的增殖和迁移。我们还发现miR-133在180对胃癌组织中被下调。 miR-133表达与肿瘤大小，浸润深度和周围器官转移呈负相关。此外，miR-133功能障碍是整体生存的独立预后因素。我们的发现可能为胃癌发生的分子机制提供新的见解，并可能有助于促进基于CDC42 / PAK的人类癌症疗法的发展。

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