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

Yue Hu1,2, Yayuan Zheng1, Mingrui Dai1

  • 1a National Engineering Laboratory for AIDS Vaccine, School of Life Sciences , Jilin University , Changchun , China.

Cell Adhesion & Migration
|July 5, 2019
PubMed

Insights

Snail2 represses E-cadherin in lung cancer by interacting with G9a and HDACs, promoting cell metastasis. Inhibiting these interactions reverses E-cadherin repression and metastasis, revealing key regulatory mechanisms.

Area of Science:

  • Molecular Oncology
  • Epigenetics
  • Cellular Carcinogenesis

Background:

  • Snail2 is recognized as a repressor of E-cadherin during cancer development.
  • The precise molecular mechanisms underlying Snail2's role in E-cadherin repression are not fully understood.
  • E-cadherin plays a crucial role in maintaining cell adhesion and suppressing tumor metastasis.

Purpose of the Study:

  • To elucidate the specific mechanisms by which Snail2 represses E-cadherin transcription.
  • To investigate the role of epigenetic modifications and protein interactions in Snail2-mediated E-cadherin repression.
  • To explore the therapeutic potential of targeting Snail2-associated regulatory pathways in lung cancer (LC) progression.

Main Methods:

  • Analysis of Snail2 expression during transforming growth factor-beta (TGF-β)-induced epithelial-mesenchymal transition (EMT) in lung cells.
  • Chromatin immunoprecipitation (ChIP) assays to assess histone modifications (H3K9 methylation, H3K4/H3K56 acetylation) at the E-cadherin promoter.
  • Co-immunoprecipitation (Co-IP) to confirm the interaction between Snail2, G9a, and histone deacetylases (HDACs).
  • In vitro assays to evaluate cell migration and invasion capabilities following Snail2 overexpression and G9a/HDACs inhibition.

Main Results:

  • Snail2 expression was significantly upregulated during TGF-β-induced EMT in lung cells.
  • Epigenetic alterations, including increased H3K9 methylation and decreased H3K4/H3K56 acetylation, were observed at the E-cadherin promoter.
  • Snail2 was found to interact with G9a and HDACs, leading to the suppression of E-cadherin transcription.
  • Overexpression of Snail2 promoted lung cell migration and invasion, effects that were significantly reversed by inhibiting G9a and HDACs.

Conclusions:

  • Snail2 represses E-cadherin transcription through interaction with the epigenetic modifiers G9a and HDACs.
  • This Snail2-G9a-HDACs axis plays a critical role in promoting cell migration, invasion, and metastasis in lung cancer.
  • Targeting the G9a- and HDACs-mediated regulation offers a potential therapeutic strategy for inhibiting Snail2-induced metastasis in lung cancer progression.
Keywords:
G9aHDACsSnail2epithelial-mesenchymal transitionlung carcinomametastasis

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