摘要
目的:探讨肿瘤坏死因子受体相关因子2(TRAF-2)和信号转导子与转录激活子6(STAT-6)在骨肉瘤发病机制中的作用,及三氧化二砷(As2O3)和血管内皮细胞生长因子(VEGF)对其表达的影响。方法:人骨肉瘤Saos-2细胞经分别加入As2O3和VEGF培养48 h后,采用实时荧光定量PCR法和流式细胞术测定TRAF2和STAT-6的表达。结果:100 ng/m L浓度的VEGF能显著上调TRAF-2及STAT-6的表达(P<0.05,P<0.01);2μmol/L以上的As2O3能显著下调TRAF-2及STAT-6的表达(P<0.05,P<0.01),它还能显著降低VEGF诱导作用(P<0.05,P<0.01)。结论:TRAF-2和STAT-6在骨肉瘤的发病机制中可能起了重要作用,VEGF具有促进疾病的进展作用,而As2O3则反之,两者具有一定的量-效关系。
AIM： To explore the possible roles of tumor necrosis factor receptor-associated factor-2（ TRAF-2） and signal transducer and activator of transcription 6（ STAT-6） in the pathogenesis of osteosarcoma,and effects of arsenic trioxide（ As2O3）and vascular endothelial growth factor（ VEGF） on human Saos-2 cell line were observed. METHODS： Human osteosarcoma Saos-2 cell line was cultured and treated with As2O3 and VEGF. After 48 hours, real-time quantitative reverse transcription polymerase chain reaction（ QRT-PCR） and flow cytometry methods were used to investigate the TRAF-2 and STAT-6 expressions. RESULTS： The expressions of TRAF-2 and STAT-6 were significantly increased in Saos-2 cell line treated with VEGF at 100 ng / m L concentration（ P〈 0. 05,P〈 0. 01,respectively）. Moreover,they were significantly decreased in Saos-2 cell line treated with As2O3 at 2 μmol / L concentration（ P〈 0. 05,P〈 0. 01,respectively）.In addition, the inducing function of VEGF on TRAF-2 and STAT-6 expressions could be inhibited significantly by As2O3（ P〈 0. 05,P〈 0. 01,respectively）. CONCLUSION： TRAF-2 and STAT-6may play an important role in pathogenesis of osteosarcoma. The osteosarcoma cell proliferation can be promoted by VEGF and inhibited by As2O3 in a dose-dependent manner.
出处
《中国临床药理学与治疗学》
CAS
CSCD
2015年第9期993-997,共5页
Chinese Journal of Clinical Pharmacology and Therapeutics
基金
温岭市科技局基金资助项目(2013-1-64)
