title: Cinobufocini inhibits NF-κB and COX-2 activation induced by TNF-α in             lung adenocarcinoma cells.
abstract: The aim of the present study was to investigate the effects of cinobufocini             on nuclear factor-κB (NF-κB), cyclooxygenase-2 (COX-2) and the production of cytokines             induced by tumor necrosis factor-α (TNF-α) in the A549 cell line. A549 cells were             incubated with cinobufocini at different concentrations for 24, 48 or 72 h. Cell             proliferation was examined by the WST-8 assay. The expression of NF-κB, COX-2             and inhibitor κBα (IκBα) was studied by western blotting. The NF-κB-dependent             luciferase rporter (3xκB-luc) was transfected for 24 h, the cells were treated             with the reagents for 24 h, and the transcriptional activity of the NF-κB promoter             was detected by a luciferase assay. The levels of IL-6 and IL-8 mRNA were detected             by reverse transcription-polymerase chain reaction. We found that cinobufocini             inhibited NF-κB p65 expression and the transcriptional activity of the NF-κB promoter             induced by TNF-α compared with the control in the nuclei of A549 cells. Moreover,             induced COX-2 expression was blocked by cinobufocini and was correlated with a             reduction in the activated p65 subunit of NF-κB. Additionally, the levels of IL-6             and IL-8 mRNA induced by TNF-α were significantly suppressed by the addition of             cinobufocini. In conclusion, these results suggest that the anti-inflammatory             effects of cinobufocini are dependent on the NF-κB/COX-2 pathway in A549 cells,             thereby providing a possible anticancer mechanism for the compound.
authors.affiliation: Cancer Institute of Traditional Chinese Medicine (TCM), Longhua Hospital, School of Life Sciences, Shanghai University of TCM, Shanghai 200032, PR China.
authors.forename: Ju-Yong
authors.initials: JY
authors.lastname: Wang
authors.forename: Ling
authors.initials: L
authors.lastname: Chen
authors.forename: Zhan
authors.initials: Z
authors.lastname: Zheng
authors.forename: Qing
authors.initials: Q
authors.lastname: Wang
authors.forename: Jing
authors.initials: J
authors.lastname: Guo
authors.forename: Ling
authors.initials: L
authors.lastname: Xu
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism*; D000077192:Adenocarcinoma of Lung; D000664:Amphibian Venoms / Q000737:chemistry / Q000494:pharmacology*; D000970:Antineoplastic Agents / Q000737:chemistry / Q000494:pharmacology*; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D051546:Cyclooxygenase 2 / Q000378:metabolism*; D004789:Enzyme Activation / Q000187:drug effects; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D015850:Interleukin-6 / Q000235:genetics; D016209:Interleukin-8 / Q000235:genetics; D008175:Lung Neoplasms / Q000378:metabolism*; D008516:Medicine, Chinese Traditional; D016328:NF-kappa B / Q000037:antagonists & inhibitors* / Q000235:genetics; D011401:Promoter Regions, Genetic; D014158:Transcription, Genetic / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
chemical_list: D000664:Amphibian Venoms; D000970:Antineoplastic Agents; D015850:Interleukin-6; D016209:Interleukin-8; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; C545813:huachansu; D051546:Cyclooxygenase 2