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.
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)
关键词
骨肉瘤
SAOS-2细胞
AS2O3
TRAF-2
STAT-6
VEGF
osteosarcoma
Sa OS-2 cell line
arsenic trioxide
tumor necrosis factor receptor-associated factor 2
signal transducer andactivator of transcription 6
vascular endothelial growth factor
