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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Main Authors: Yue Hu, Yayuan Zheng, Mingrui Dai, Jiaxin Wu, Bin Yu, Haihong Zhang, Wei Kong, Hui Wu, Xianghui Yu
Format: Article
Language:English
Published: Taylor & Francis Group 2019-01-01
Series:Cell Adhesion & Migration
Subjects:
Online Access:http://dx.doi.org/10.1080/19336918.2019.1638689
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author Yue Hu
Yayuan Zheng
Mingrui Dai
Jiaxin Wu
Bin Yu
Haihong Zhang
Wei Kong
Hui Wu
Xianghui Yu
author_facet Yue Hu
Yayuan Zheng
Mingrui Dai
Jiaxin Wu
Bin Yu
Haihong Zhang
Wei Kong
Hui Wu
Xianghui Yu
author_sort Yue Hu
collection DOAJ
description 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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spelling doaj.art-8c3aee3c5d6b4c7b8369afaa30bf4f962022-12-22T00:04:43ZengTaylor & Francis GroupCell Adhesion & Migration1933-69181933-69262019-01-0113128429110.1080/19336918.2019.16386891638689Snail2 induced E-cadherin suppression and metastasis in lung carcinoma facilitated by G9a and HDACsYue Hu0Yayuan Zheng1Mingrui Dai2Jiaxin Wu3Bin Yu4Haihong Zhang5Wei Kong6Hui Wu7Xianghui Yu8Jilin UniversityJilin UniversityJilin UniversityJilin UniversityJilin UniversityJilin UniversityJilin UniversityJilin UniversityJilin UniversitySnail2 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.http://dx.doi.org/10.1080/19336918.2019.1638689snail2g9ahdacsepithelial-mesenchymal transitionmetastasislung carcinoma
spellingShingle Yue Hu
Yayuan Zheng
Mingrui Dai
Jiaxin Wu
Bin Yu
Haihong Zhang
Wei Kong
Hui Wu
Xianghui Yu
Snail2 induced E-cadherin suppression and metastasis in lung carcinoma facilitated by G9a and HDACs
Cell Adhesion & Migration
snail2
g9a
hdacs
epithelial-mesenchymal transition
metastasis
lung carcinoma
title Snail2 induced E-cadherin suppression and metastasis in lung carcinoma facilitated by G9a and HDACs
title_full Snail2 induced E-cadherin suppression and metastasis in lung carcinoma facilitated by G9a and HDACs
title_fullStr Snail2 induced E-cadherin suppression and metastasis in lung carcinoma facilitated by G9a and HDACs
title_full_unstemmed Snail2 induced E-cadherin suppression and metastasis in lung carcinoma facilitated by G9a and HDACs
title_short Snail2 induced E-cadherin suppression and metastasis in lung carcinoma facilitated by G9a and HDACs
title_sort snail2 induced e cadherin suppression and metastasis in lung carcinoma facilitated by g9a and hdacs
topic snail2
g9a
hdacs
epithelial-mesenchymal transition
metastasis
lung carcinoma
url http://dx.doi.org/10.1080/19336918.2019.1638689
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