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Updated: Jan 12, 2026
Using Nicotine in a Silica-Exposed Mouse Model to Promote Lung Epithelial-Mesenchymal Transition
Published on: March 3, 2023
The α5-nAChR/GINS4 axis contributed to nicotine-promoted lung adenocarcinoma progression
Zengping Wang1, Jiaying Cai2, Mengdan Yang1
1Department of Medical Laboratory, Shandong Second Medical University, Weifang, 261053, Shandong, China.
Abstract:
The α5-nicotinic acetylcholine receptor (α5-nAChR) is implicated in nicotine-driven proliferation of lung cancer cells. GINS4 functions as a regulatory factor of the G1/S transition and DNA replication dynamics, closely linking it to proliferative capacity. Profiling of CHRNA5, the gene encoding α5-nAChR, indicated that silencing CHRNA5 reduced GINS4 expression. The mechanistic relationship between α5-nAChR and GINS4 in lung adenocarcinoma (LUAD), however, has not been fully clarified. Analysis in this study revealed that α5-nAChR expression correlated with GINS4 levels, smoking status, and overall survival. In vitro experiments demonstrated that α5-nAChR mediates nicotine-induced GINS4 expression via STAT3, thereby enhancing LUAD cell proliferation, migration, and invasion. The α5-nAChR/GINS4 axis was further validated in both mouse xenograft models and human LUAD tissue samples. Collectively, the results indicate the existence of a novel α5-nAChR/GINS4 signaling pathway contributing to nicotine-associated LUAD progression.
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