Snail2 induced E-cadherin suppression and metastasis in lung carcinoma facilitated by G9a and HDACs

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 acetylati...

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Detalles Bibliográficos
Autores principales: Hu, Yue, Zheng, Yayuan, Dai, Mingrui, Wu, Jiaxin, Yu, Bin, Zhang, Haihong, Kong, Wei, Wu, Hui, Yu, Xianghui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2019
Materias:
Short Communication
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6629185/
https://www.ncbi.nlm.nih.gov/pubmed/31271097
http://dx.doi.org/10.1080/19336918.2019.1638689
Descripción
Sumario: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.

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