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Abstract Title:

Inhibitory effect of sinomenine on lung cancer cells via negative regulation ofα7 nicotinic acetylcholine receptor.

Abstract Source:

J Leukoc Biol. 2021 04 ;109(4):843-852. Epub 2020 Jul 29. PMID: 32726882

Abstract Author(s):

Shasha Bai, Wenhao Wen, Xuenan Hou, Jiexiu Wu, Lang Yi, Yingkun Zhi, Yanjun Lv, Xiaoqin Tan, Liang Liu, Peixun Wang, Hua Zhou, Yan Dong

Article Affiliation:

Shasha Bai

Abstract:

Lung cancer is the leading cause of cancer deaths worldwide, with a high morbidity and less than 20% survival rate. Therefore, new treatment strategies and drugs are needed to reduce the mortality of patients with lung cancer.α7 nicotinic acetylcholine receptor (α7 nAChR), as a receptor of nicotine and its metabolites, is a potential target for lung cancer treatment. Our previous studies revealed that sinomenine plays anti-inflammation roles via α7 nAChR and down-regulates the expression of this receptor, thus increasing the inflammatory response. Hence, sinomenine is possibly a natural ligand of this receptor. In the present study, the effects of sinomenine on lung cancer A549 cells and tumor-bearing mice were determined to investigate whether this alkaloid has an inhibitory effect on lung cancer via α7 nAChR.CCK-8 assay, wound-healing test, and flow cytometry were performed for cell proliferation, cell migration, and apoptosis analysis in vitro, respectively. Xenograft mice were used to evaluate the effects of sinomenine in vivo. Results showed that sinomenine decreased cell proliferation and migrationabilities but increased the percentage of apoptotic cells. Tumor volume in tumor-bearing mice was significantly reduced after sinomenine treatment compared with that in the vehicle group mice (p < 0.05). Furthermore, the effects of sinomenine were abolished by the α7 nAChR antagonist mecamylamine and the allosteric modulator PNU-120596, but no change occurred when the mice were pretreated with the muscarinic acetylcholine receptor antagonist atropine. Meanwhile, sinomenine suppressed α7 nAChR expression in vitro and in vivo, as well as the related signaling molecules pERK1/2 and ERK1/2 and the transcription factors TTF-1 and SP-1. By contrast, sinomenine up-regulated the expression of another transcription factor, Egr-1. These effects were restricted by mecamylamine and PNU but notby atropine. Results suggested that sinomenine can inhibit lung cancer via α7 nAChR in a negative feedback mode.

Study Type : Animal Study, In Vitro Study
Additional Links
Pharmacological Actions : Antiproliferative : CK(6801) : AC(5032)

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