血管内皮生长因子在六价铬诱导的肺支气管上皮细胞Beas-2B恶性转化中的作用

Abstract
Figure/Table
References
Related Citation (9)

Download: PDF (4715 KB) HTML (1 KB)
Export: BibTeX | EndNote (RIS)

Abstract Objective: To explore the biological role of vascular endothelial growth factor (VEGF) in migration, invasion and angiogenesis during the malignant transformation of human bronchial epithelial cells Beas2B induced by hexavalent chromium, and to explore whether VEGF can regulate migration and invasion by influencing the expression of migration and invasionrelated proteins at the protein and molecular levels. Methods: VEGF expression was up-regulated or down-regulated by recombinant VEGF overexpression plasmid and siRNA interference, respectively. And then detected the expression of VEGF and migration and invasion related proteins by western blotting, and the migration and invasion abilities were measured by wound healing, Transwell and immunofluorescence assays, and angiogenesis ability was evaluated by tube formation test. Results: Overexpression of VEGF by recombinant VEGF plasmid up-regulated the expression of VEGF, matrix metalloproteinase-9, phosphorylated activated form of focal adhesion kinase and Src protein, and down-regulated E-cadherin expression in malignant transformed cells; Overexpression of VEGF by recombinant VEGF plasmid also enhanced the migration, invasion and angiogenesis ability of malignant transformed cells; The results of siRNA interference were contrary to those of VEGF overexpression. Conclusion: By influencing the expression of migration/invasion-related proteins, VEGF regulates cell migration, invasion and angiogenesis, and participates in the carcinogenesis induced by hexavalent chromium.

Received: 16 May 2019

	Service

	E-mail this article
	Add to my bookshelf
	Add to citation manager
	E-mail Alert
	RSS
	Articles by authors

Cite this article:

URL:

http://zzs.ujs.edu.cn/xbyxb/EN/ OR http://zzs.ujs.edu.cn/xbyxb/EN/Y2019/V29/I05/369

［1］Siegel R, Naishadham D, Jemal A. Cancer statistics, 2012\[J\]. CA Cancer J Clin, 2012, 62(1):10-29.
［2］Proctor DM. Inhalation cancer risk assessment of hexavalent chromium based on updated mortality for Painesville chromate production workers\[J\]. J Expo Sci Env Epid, 2016, 26(2):224-231.
［3］Dayan AD, Paine AJ. Mechanisms of chromium toxicity, carcinogenicity and allergenicity: review of the literature from 1985 to 2000\[J\]. Hum Exp Toxicol, 2001, 20(9):439-451.
［4］Korpanty G, Smyth E, Sullivan LA, et al. Antiangiogenic therapy in lung cancer: focus on vascular endothelial growth factor pathway\[J\]. Exp Biol Med, 2010, 235(1):3-9.
［5］Ramon ADM, Costa BM, Rui MR, et al. Insights into angiogenesis in nonsmall cell lung cancer: molecular mechanisms, polymorphic genes, and targeted therapies\[J\]. Recent Pat Anticancer Drug Discov, 2012, 7(1):118-131.
［6］Bonnesen B, Pappot H, Holmstav J, et al. Vascular endothelial growth factor A and vascular endothelial growth factor receptor 2 expression in nonsmall cell lung cancer patients: relation to prognosis\[J\]. Lung Cancer, 2009, 66(3):314-318.
［7］Frezzetti D, Gallo M, Maiello MR, et al. VEGF as a potential target in lung cancer\[J\]. Expert Opin Ther Tar, 2017, 21(10):959-966.
［8］Johnson DH, Schiller JH, Bunn PA Jr. Recent clinical advances in lung cancer management\[J\]. J Clin Oncol, 2014, 32(10):973-982.
［9］陈丽蓉, 陈小罗, 严志辉,等. 土壤中重金属污染物铬的迁移转化及治理\[J\]. 科技创新导报, 2011 (33):122-123.
［10］张子栋. 六价铬毒性作用及其影响因素\[J\]. 生物技术世界, 2013(8):71.
［11］孙姣姣. 水中的重金属污染——铬\[J\]. 金田,2012，11：306.
［12］Arita A, Costa M. Handbook of Epigenetics\[M\]. Amsterdam: Elsevier, 2011：459-476.
［13］Zhuo Z, Poyil P, Amit B, et al. Role of reactive oxygen species in arsenicinduced transformation of human lung bronchial epithelial (Beas2B) cells\[J\]. Biochem Bioph Res Co, 2015, 456(2):643-648.
［14］Ganapathy S, Li P, Lafontant J, et al. Chromium IV exposure, via src/Ras signaling, promotes cell transformation\[J\]. Mol Carcinog, 2017, 56(7):1808-1815.
［15］Rodrigues CF, Urbano AM, Matoso E, et al. Human bronchial epithelial cells malignantly transformed by hexavalent chromium exhibit an aneuploid phenotype but no microsatellite instability\[J\]. Mutat Res, 2009, 670(1-2):42-52.