Snail2 is a repressor of E-cadherin during carcinogenesis; however, the specific mechanisms involved in this process remain largely unknown. Here, we determined that Snail2 was highly increased during TGF-β-induced EMT process in lung cells. H3K9 methylation was up-regulated and H3K4/H3K56 acetylation were down-regulated at the E-cadherin promoter. Snail2 interacted with G9a and HDACs to exert suppression of E-cadherin transcription. Overexpression of Snail2 enhanced the migration and invasion ability, whereas G9a and HDACs inhibition significantly reversed this effect. Our study demonstrated the importance of G9a- and HDACs-mediated regulation during Snail2-induced E-cadherin repression and metastasis during LC progression.

中文翻译：

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Snail2诱导的G9a和HDAC促进了E-cadherin在肺癌中的抑制和转移。

Snail2在致癌过程中是E-钙粘蛋白的阻遏物。但是，此过程中涉及的具体机制仍然未知。在这里，我们确定Snail2在TGF-β诱导的肺细胞EMT过程中高度增加。在E-钙粘着蛋白启动子上，H3K9甲基化被上调，而H3K4 / H3K56乙酰化被下调。Snail2与G9a和HDAC相互作用，以抑制E-钙粘蛋白的转录。Snail2的过表达增强了迁移和侵袭能力，而G9a和HDAC的抑制作用则显着逆转了这一作用。我们的研究证明了在Snail2诱导的E-钙粘蛋白抑制和LC进展过程中转移过程中，G9a和HDACs介导的调节的重要性。