Nicotine effects on proliferation and the bombesin-like peptide autocrine system in human small cell lung carcinoma SHP77 cells in culture
2000; Elsevier BV; Volume: 29; Issue: 1 Linguagem: Inglês
10.1016/s0169-5002(00)00117-3
ISSN1872-8332
AutoresJohn S. Novak, Antonio Escobedo-Morse, Kim Kelley, Dorothy Boose, Donna Kautzman-Eades, Melissa Meyer, Madeleine Kane,
Tópico(s)Antimicrobial Peptides and Activities
ResumoTo 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.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.Nicotine significantly stimulated the growth of human SCLC SHP77 and NCI-H865 cells, but not BEAS 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.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 bombesin-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.
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