Nicotine effects on proliferation and the bombesin-like peptide autocrine system in human small cell lung carcinoma SHP77 cells in culture

Nicotine effects on proliferation and the bombesin-like peptide autocrine system in human small cell lung carcinoma SHP77 cells in culture
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DOI:
10.1016/s0169-5002(00)00117-3
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发表时间:
2000-07-01
期刊:
影响因子:
5.3
通讯作者:
Kane, MA
Kane, MA
中科院分区:
医学2区
文献类型:
--
作者:
Novak, J;Escobedo-Morse, A;Kane, MA

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目的:与作为非神经内分泌对照的非恶性人支气管上皮 BEAS 2B 细胞相比,确定尼古丁是否影响人小细胞肺癌 (SCLC) SHP77 细胞中铃蟾肽样肽自分泌系统的增殖和表达。方法:在添加不同浓度尼古丁的限定成分无血清培养基中培养人肺细胞,培养不同时间。通过细胞计数和比色测定测量增殖,通过特异性结合测定和定量竞争PCR测定铃蟾肽样肽受体表达,并通过ELISA测定铃蟾肽样肽。结果:尼古丁显着刺激人 SCLC SHP77 和 NCI-H865 细胞的生长,但不刺激 PEAS 2B 细胞的生长。在 SHP77 细胞或 BEAS 2B 细胞中,铃蟾肽样肽受体特异性结合和 mRNA 表达不受尼古丁暴露的影响。观察到 SHP77 细胞铃蟾肽样肽含量增加。结论:人 SCLC SHP77 细胞表达铃蟾肽样肽自分泌系统的成分。尼古丁存在下增殖的增加可能部分是由于在尼古丁中培养的 SHP77 中伯恩贝辛样肽水平的增加。尼古丁对非恶性肺神经内分泌细胞的影响可能为了解尼古丁本身如何促进肺癌发生提供更多见解。 (C) 2000 年,爱思唯尔科学爱尔兰有限公司出版。
Objectives: To determine whether nicotine affects the proliferation and expression of the bombesin-like peptide autocrine system in human small cell lung carcinoma (SCLC) SHP77 cells compared with nonmalignant human bronchial epithelial BEAS 2B cells as non-neuroendocrine controls. Methods: Human lung cells were cultured in defined serum-free medium with various concentrations of nicotine added for various times. Proliferation was measured by cell counts and colorimetric assay, bombesin-like peptide receptor expression was assayed by specific binding assays and quantitative competitive PCR, and bombesin-like peptides determined by ELISA. Results: Nicotine significantly stimulated the growth of human SCLC SHP77 and NCI-H865 cells, but not PEAS 2B cells. Bombesin-like peptide receptor specific binding and mRNA expression were not affected by nicotine exposure in SHP77 cells or BEAS 2B cells. An increase in SHP77 cellular bombesin-like peptide content was observed. Conclusions: Human SCLC SHP77 cells express the components of the bombesin-like peptide autocrine system. Increased proliferation in the presence of nicotine may be due in part to increased levels of bornbesin-like peptides in SHP77 cultured in nicotine. Nicotine effects on nonmalignant pulmonary neuroendocrine cells may provide additional insight into how nicotine itself may promote lung carcinogenesis. (C) 2000 Published by Elsevier Science Ireland Ltd.