摘要
目的探讨MTSS1基因在骨肉瘤组织中的表达情况,对骨肉瘤细胞增殖、迁移和侵袭能力的影响及其机制。方法qRT-PCR、Western blot和免疫组化染色分别检测骨肉瘤组织及其对应的癌旁组织样本中MTSS1的mRNA和蛋白表达水平。构建MTSS1表达载体在骨肉瘤细胞株MG63中过表达MTSS1,采用CCK-8法检测细胞增殖情况,流式细胞术检测细胞凋亡情况;通过Transwell细胞迁移和侵袭实验分别检测对细胞迁移和侵袭能力的影响;检测MMP2和MMP9的表达情况<结果骨肉瘤组织中MTSS1mRNA和蛋白表达显著低于癌旁组织MTSS1高表达能够抑制MG63细胞的增殖,抑制细胞凋亡。MTSS1表达上调显著降低细胞的迁移和侵袭能力MG63细胞中过表达MTSS1可以降低MMP2和MMP9的表达。结论MTSS1基因在骨肉瘤中低表达,MTSS1能够降低MG63细胞的增殖并促进细胞凋亡,可能通过抑制MMP2和MMP9的表达调控骨肉瘤的侵袭和转移。
Objective To investigate the expression of MTSS1 gene in osteosarcoma tissues,the impact of MTSS1 overexpression on proliferation,migration and invasion in osteosarcoma cells and the related mechanism. Methods qRT-PCR,Western blot and immunohistochemistry were used to detect the mRNA and protein expression of MTSS1 in osteosarcoma and matched adjacent normal tissues. MTSS1 was overexpressed in osteosarcoma cell line MG63 by transfected into constructed MTSS1 expression vector,then the proliferation and apoptosis were detected by CCK-8 and flow cytometry,respectively. Cell migration and invasion were assessed by transwell migration and matrigel invasion assay. The expression of MMP2 and MMP9 were also detected. Results The mRNA and protein expression of MTSS1 in osteosarcoma tissues were significant lower than those in paired adjacent tissues. MTSS1 overexpression inhibited the proliferation of MG63 cells and promoted its apoptosis. Up-regulated expression of MTSS1 significantly reduced the cell migration and invasion. MMP2 and MMP9 expression were both decreased in MG63 cells transfected with MTSS1 overexpression vector. Conclusion MTSS1 expression is down-regulated in osteosarcoma. The overexpression of MTSS1 can decrease the proliferation and promote the apoptosis of MG63 cells,and it may regulate migration and invasion via inhibiting MMP2 and MMP9 expression in osteosarcoma.
作者
谢杏苗
黄永军
冯璐
刘晓春
江奕恒
余超群
XIE Xingmiao;HUANG Yongjun;FENG Lu;LIU Xiaochun;JIANG Yiheng;YU Chaoqun(Guangzhou Panyu Shiji Peoples Hospital, Guangzhou, 511450, China)
出处
《现代医院》
2019年第8期1179-1184,共6页
Modern Hospitals
基金
广东省医学科研基金(A2016009)