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Zhu, Ping; Kang, Guiyu; Jiao, Yang; Gui, Chengzhi; Fan, Huiping; Li, Xiangying; Jia, Yanfei; Zhang, Lulu; Ma, Xiaoli
Human cell : official journal of Human Cell Research Society, 07/2022, Letnik: 35, Številka: 4Journal Article
α 5 nicotinic acetylcholine receptor ( α 5-nAChR) is associated with the progression of smoking-related lung adenocarcinoma (LUAD), but the molecular mechanism is unclear. Programmed death ligand 1 (PD-L1) is encoded by the CD274 gene, which not only inhibits the immune system, but also plays a unique role in tumor growth and metastasis. Here, we gained important insights into the underlying mechanism between α 5-nAChR and PD-L1 in LUAD progression. α 5-nAChR was overexpressed in various histological subtypes, cancer stages and metastasis statuses of LUAD. The group that coexpressed α 5‐nAChR and PD-L1 had a worse prognosis than the other subgroups at different stages of LUAD lymph node metastasis. The expression of α 5‐nAChR and PD-L1 was associated with epithelial–mesenchymal transition (EMT) marker CDH2. In vitro, α 5-nAChR mediated nicotine-induced PD-L1 expression via STAT3 and the expression of EMT markers. Downregulation of α 5-nAChR and/or PD-L1 inhibited EMT marker expression, cell proliferation, migration and invasion compared to silencing α 5-nAChR or PD-L1 alone in LUAD cells. Furthermore, α 5-nAChR expression was associated with PD-L1 and EMT marker expression in mouse xenograft models. These results highlight that α 5-nAChR mediates STAT3/PD-L1 signaling, which contributes to cell migration and invasion. Therefore, our study may reveal a new interaction between α 5-nAChR and PD-L1 that is involved in tumor cell growth and progression in LUAD, which may be a promising target for NSCLC diagnosis and immunotherapy.
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Leto | Faktor vpliva | Izdaja | Kategorija | Razvrstitev | ||||
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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