title: The molecular mechanism of luteolin-induced apoptosis is potentially             related to inhibition of angiogenesis in human pancreatic carcinoma cells.
abstract: Luteolin has been shown to have a strong anticancer effect on various cancer             models via programmed cell death (apoptosis). However, the fundamental mechanisms             of these effects are still unclear. In the present study, we examined the question             of whether or not luteolin can inhibit proliferation of pancreatic carcinoma cells,             via apoptosis. We used three human pancreatic carcinoma cell lines, PANC-1, CoLo‑357             and BxPC-3 in our study. In luteolin-treated pancreatic carcinoma cells, typical             features of apoptosis were observed. Luteolin increased the expression of the             pro-apoptotic protein Bax and decreased the expression of the anti-apoptotic protein             Bcl-2, with a concomitant increase in the levels of caspase-3 and cleaved PARP             after treatment for 24 h. Luteolin inhibited HUVEC proliferation and vessel growth             in CAM in vivo. In addition, the concentration of VEGF in the conditioned medium             from human pancreatic carcinoma cells was downregulated by luteolin. Pancreatic             carcinoma cells, pretreated with luteolin, could decrease the capillary-like structure             formation by HUVEC, which was analyzed by a co-culture system. The abatement of             VEGF secretion was related to the inhibition of VEGF mRNA expression, which may             be regulated by inhibiting the transcription activity of nuclear transcription             factor NF-κB.
authors: Laboratory of Cellular and Molecular Biology, Jiangsu Province Academy of Traditional Chinese Medicine, Nanjing 210028, PR China.
authors: Xueting
authors: X
authors: Cai
authors: Wuguang
authors: W
authors: Lu
authors: Tingmei
authors: T
authors: Ye
authors: Min
authors: M
authors: Lu
authors: Jianhua
authors: J
authors: Wang
authors: Jiege
authors: J
authors: Huo
authors: Shihui
authors: S
authors: Qian
authors: Xiaoning
authors: X
authors: Wang
authors: Peng
authors: P
authors: Cao
mesh_terms: D020533:Angiogenesis Inhibitors / Q000494:pharmacology*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D059447:Cell Cycle Checkpoints / Q000187:drug effects; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D002642:Chick Embryo; D049033:Chorioallantoic Membrane / Q000187:drug effects; D018920:Coculture Techniques; D061307:Human Umbilical Vein Endothelial Cells / Q000187:drug effects; D006801:Humans; D047311:Luteolin / Q000494:pharmacology*; D048670:MAP Kinase Kinase 4 / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D009389:Neovascularization, Pathologic / Q000188:drug therapy*; D010190:Pancreatic Neoplasms / Q000098:blood supply / Q000188:drug therapy* / Q000473:pathology; D010766:Phosphorylation; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics / Q000378:metabolism
chemical_list: D020533:Angiogenesis Inhibitors; D016328:NF-kappa B; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D048670:MAP Kinase Kinase 4; D047311:Luteolin