摘要
Sulfiredoxin(SRX)作为一种重要的抗氧化蛋白质,最近研究发现其对某些肿瘤细胞生物学行为及细胞恶性转化有重要作用,而SRX对宫颈癌细胞恶性生物学行为有何影响尚未见报道.本研究选取宫颈癌He La细胞株,分别设为Wild-type(WT)组,Non-target(NT)组,Knock-down(KD)组.利用siRNA技术干扰SRX基因在He La细胞中的内源性表达,采用MTT法、平板克隆形成实验、Transwell实验、流式细胞术分别检测肿瘤细胞增殖力、浸润、迁移能力、细胞凋亡情况,并分别用3组He La细胞上清液处理人脐静脉内皮细胞,观察各组条件培养基对内皮细胞血管形成能力的影响.结果表明,与两对照组比较,SRX干扰组细胞增殖力、浸润、迁移力显著降低,且干扰组上清使内皮细胞体外血管形成能力也明显下降(P<0.05),而凋亡率则明显增加(P<0.05).而两对照组之间结果均无显著差异(P>0.05).实验结果表明,SRX基因对宫颈癌He La细胞恶性生物学行为具有促进作用,说明SRX可能与宫颈癌恶性进展有密切关系.
Sulfiredoxin （SRX） is an important antioxidant activity protein; recent studies showed its effects on the biological behaviors in some human cancer cells and normal cell malignant transformation. However, whether there is a relationship between SRX and the malignant biological behavior of cervical carcinoma cells has not been reported. To solve this problem, HeLa cells have been chosen and divided into three groups： wild-type （WT） group, non-target （NT） group and silencing （KD） group, siRNA technique was performed to reduce SRX endogenous expression. Cell proliferation was determined by the MTT and plate clone formation assay. Flow cytometry and Transwell chamber assay were used to detect cell apoptosis ratio and metastasis ability of each group. The angiogenesis ability in vitro was measured through observing the tube formation of EA. hy926 cells were cultured in three dimensional medium after treated EA. hy926 cells with the supernatant of each group. We found that compared with controls, the cell proliferation, migration and angiogenic abilities were decreased and cell apoptosis ratio was increased obviously in KD group （P 〈 0.05） , while there was no statistical difference between controls of these data （P 〉 0.05）. Our results indicated that SRX was involved in promoting the progression of malignant biological behavior of HeLa cells. SRX was speculated to affect the progression of cervical cancer.
出处
《中国生物化学与分子生物学报》
CAS
CSCD
北大核心
2015年第3期274-282,共9页
Chinese Journal of Biochemistry and Molecular Biology
作者简介
联系人 Tel：023-89011090；E-mail：15310918845@163．com
