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?5-nAChR contributes to epithelial-mesenchymal transition and metastasis by regulating Jab1/Csn5 signalling in lung cancer.

ABSTRACT: Recent studies have showed that ?5 nicotinic acetylcholine receptor (?5-nAChR) is closely associated with nicotine-related lung cancer. Our previous studies also demonstrated that ?5-nAChR mediates nicotine-induced lung carcinogenesis. However, the mechanism by which ?5-nAChR functions in lung carcinogenesis remains to be elucidated. Jab1/Csn5 is a key regulatory factor in smoking-induced lung cancer. In this study, we explored the underlying mechanisms linking the ?5-nAChR-Jab1/Csn5 axis with lung cancer epithelial-mesenchymal transition (EMT) and metastasis, which may provide potential therapeutic targets for future lung cancer treatments. Our results demonstrated that the expression of ?5-nAChR was correlated with the expression of Jab1/Csn5 in lung cancer tissues and lung cancer cells. ?5-nAChR expression is associated with Jab1/Csn5 expression in lung tumour xenografts in mice. In vitro, the expression of ?5-nAChR mediated Stat3 and Jab1/Csn5 expression, significantly regulating the expression of the EMT markers, N-cadherin and Vimentin. In addition, the down-regulation of ?5-nAChR or/and Stat3 reduced Jab1/Csn5 expression, while the silencing of ?5-nAChR or Jab1/Csn5 inhibited the migration and invasion of NSCLC cells. Mechanistically, ?5-nAChR contributes to EMT and metastasis by regulating Stat3-Jab1/Csn5 signalling in NSCLC, suggesting that ?5-nAChR may be a potential target in NSCLC diagnosis and immunotherapy.


PROVIDER: S-EPMC7028847 | BioStudies | 2020-01-01

REPOSITORIES: biostudies

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