三氧化二砷对VEGF诱导人骨肉瘤SaOS-2细胞TRAF-2和STAT-6表达的影响  被引量:2

Effects of Arsenic Trioxide on the Expression of TRAF-2 and STAT-6 on Human Osteosarcoma SaOS-2 Cell Line Induced by VEGF

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作  者:吴永辉[1] 林晓[1] 罗冬娇[2] 钟永翔 王恩智[3] 王鑫华[3] 

机构地区:[1]浙江省台州市中西医结合医院骨科,台州317523 [2]杭州师范大学医学院检验系,杭州311121 [3]浙江省台州市中西医结合医院检验科,台州317523

出  处:《浙江中西医结合杂志》2016年第3期215-218,共4页Zhejiang Journal of Integrated Traditional Chinese and Western Medicine

基  金:浙江省自然基金资助项目(No.LY13H080006);浙江省温岭市科技局基金资助项目(No.2013-1-64)

摘  要:目的通过观察三氧化二砷(As2O3)对血管内皮生长因子(VEGF)诱导人骨肉瘤Sa OS-2细胞肿瘤坏死因子受体相关因子(TRAF-2)和信号转导子与转录激活子(STAT-6)表达的影响,探讨As2O3治疗骨肉瘤的作用机制。方法分别采用CCK8法、实时荧光定量PCR法和流式细胞术测定细胞生长抑制率、TRAF2和STAT-6的表达。结果 2μmol/L的As2O3对Sa OS-2细胞的生长抑制率达57%(0.57±0.03比0)(P<0.01),使VEGF诱导作用显著降低(0.42±0.02)(P<0.05),TRAF-2及STAT-6的表达也显著下降(分别为:149.00±7.21比167.33±8.02;1.29±0.12比2.53±0.67)(P均<0.05)。结论 As2O3可能通过TRAF-2和STAT-6途径对Sa OS-2细胞的生长呈剂量相关的抑制作用。Objective To investigate the effect of arsenic trioxide(As2O3)on the expression of tumor necrosis factor receptor-associated factor 2(TRAF-2)and signal transducer andactivator of transcription 6(STAT-6)on human osteosarcoma Sa OS-2 cell line induced by vascular endothelial growth factor(VEGF),in an attempt to explore the mechanism of As2O3 treating human osteosarcoma.Methods CCK8 assay,real-time quantitative reverse transcription polymerase chain reaction(QRT-PCR)and flow cytometry methods were used to determine the inhibition rate and expression levels of TRAF-2 and STAT-6 on osteosarcoma Sa OS-2 cell line after treatment with As2O3.Results Treated with As2O3 of 2 μmol/L,the inhibition ratio of SaOS-2 cell line reached 57%(0.57±0.03 vs 0,P〈0.01)and the induction function of VEGF was notably depressed(0.42±0.02,P〈0.05).The expression levels of TRAF-2(149.00±7.21 vs 167.33±8.02)and STAT-6(1.29±0.12 vs 2.53±0.67)significantly decreased(all P〈0.05).Conclusion The inhibition function of As2O3 on osteosarcoma cell proliferation is in a dose-dependent manner,which may be related to TRAF-2 and STAT-6 pathway.

关 键 词:骨肉瘤 SAOS-2细胞 AS2O3 TRAF-2 STAT-6 VEGF 

分 类 号:R738.1[医药卫生—肿瘤]

 

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