Title : Low-Dose Nicotine Activates EGFR Signaling via α5-nAChR and Promotes Lung Adenocarcinoma Progression.

Pub. Date : 2020 Sep 17

PMID : 32957649






4 Functional Relationships(s)
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1 Low-Dose Nicotine Activates EGFR Signaling via alpha5-nAChR and Promotes Lung Adenocarcinoma Progression. Nicotine cholinergic receptor nicotinic alpha 4 subunit Homo sapiens
2 In LAC cell lines alpha 5-nAChR interacts with epidermal growth factor receptor (EGFR), positively regulates EGFR pathway, enhances the expression of epithelial-mesenchymal transition markers, and is essential for low-dose nicotine-induced EGFR phosphorylation. Nicotine cholinergic receptor nicotinic alpha 4 subunit Homo sapiens
3 Functionally, low-dose nicotine requires alpha 5-nAChR to enhance cell migration, invasion, and proliferation. Nicotine cholinergic receptor nicotinic alpha 4 subunit Homo sapiens
4 Our data identified alpha 5-nAChR as an essential mediator for low-dose nicotine-dependent LAC progression possibly through signaling crosstalk with EGFR, supporting the involvement of environmental smoke in tumor progression in LAC patients. Nicotine cholinergic receptor nicotinic alpha 4 subunit Homo sapiens