VEGF基因沉默联合唑来膦酸抑制胃癌细胞增殖和迁移的机制 - 论文

现代肿瘤医学 20/ 年 4 月 第 2 卷第 20 期 MODERN ONCOLOGY, Oh 20/, VOL. 2, No 20? 3597 ?VEGF基因沉默联合卩坐来麟酸抑制胃癌细胞增殖和迁移的机制李自显7徐刚2,王亚楠2,杨文义5Mechanisms of targeting VEGF gene combined with zoledronic acid on proliferation and migration ot hepaacellulnr corcinoma cellsLi Zixisn1 ,Xu Gang2 , Wang Yanan2 * , Yang We/yi51 Department cf Digestive Medicine Onyang District Hospital, Puyang City, Henan Anyang 455400, Ohina ； Department of Digestive Medi-

cine ,Secoog A—ed Hospital of Zhengzhoo University, Henaa Zhengzhoo 454000, Ohina ；6 Departmeat of Digestive Medicias, FirsP affili-ated Hospital o Henan Universita, Henan Kaifeng 474000, China.【Abstracl, Objective: To ivvesti/te the ekects of mryeteC inPibiCoo of VEGF gene combiuek with zoU/moic scib

oo pmOfem/oo ,migm/oo and STAT3 sicna/ny is Ue/atocellulso camiuoms cells. Method：: 1i - VEGF was transfect-

eC into BGC - 843 cells by LipofecmmipeTM2200, sud the tmnsfectioo ekects were hetecteC by RT - PCR and Western

bUt. After tmnsfectioo ,diRemvt coocentra/oos of zoU/moic acib were use/ to co cyOuro for 43 0. The ekect of si - VEGF combiuek with zoU/moic acid oo the proliferaVoo of BGC -843 cells was hetecteC by MTT,and IC57 of zolc-

drooio scib was hetecteC. The cells were ravdomly hiviSek into si - NC gropp (WansfecteC uega/ve cootrol I : si - NC

+ zoU/moic scib gropp ( Vtco tmnsfectioo of uegative cootrol, zoU/moic scib treatment- : si - VEGF gropp ( tmus- fecteC si - VEGF) and si - VEGF + zoU/moic scib gropp ( Vtco tmnsfectioo of si - VEGF, zoU/moic scib treat-

ment) .The cell iuvasHo and migra/oo aSiOty were hetecteC by TmusweX cell experiment, avd the expmssioo of STAT3 . p - STAT3 and MMP - 4 proteids is the cells were measure/ by Western bUt. Results: After tmnsfec/ou of si

-VEGF,the expmssioo of VEGF mRNA and proteid is BGC -843 cells was downregulatek successfully. The indibi- tory effect of si - VEGF combiued with zoledrooio acib oo the prolifera/oo of BGC - 843 cells was si/iifihnPy highco

thau that of zoU/moic scib aUoe,and the IC57 of zoU/moic acib was 64. 94 ^moUP. CompamS with the si - NC

gmpp,the uumbers of invasive cells and migmtom cells is the si - NC + zoledrooio acib gmpp,the si - VEGF gropp and the si - VEGF + zoU/moic acib pmap were hecmaseC oXvioasly. and the expmssioo、of p - STAT3 avd MMP - 4

proteid were reSucek oPvHpsly,bpt the diRerevces of STAT3 expmssioo were uct oPvioxs. Amoog them,the ekect of si

-VEGF + zole/rooic acib propp was si/iificanVy highco thau that of si - NC + zoU/moic scib pmap co si - VEGF pmap. Conclusion ： The inPibiCoo of VEGF gene and zoU/moic acib can inhibit the prolifera/oo avd mipratioo of

Ue/atoms carcinoma cell, and the mechanism may be relate/ to the inhibiCou of STAT3 signa/np pathway.【Key wordsiUe/atoms camiuoms ceX,VEGF gene,zoUSmoic acid,ceU prolifera/oo,STAT3 si/ia/ny pathwayMoheru Oucology 20/,27(20) ：3597 -360)【摘要】目的:探讨靶向抑制VEGF基因联合瞠来瞬酸对胃癌细胞增殖、迁移及STAT3信号通路的影响。方 法:采用LipofecmmipeTM2200将si- VEGF转染至胃癌BGC -843细胞中，以RT - PCR和Western blot检测其

转染效果。转染后，加入不同浓度的瞠来瞬酸共同培养48 U,MTT法检测-5 - VEGF联合瞠来瞬酸对BGC - 843细胞增殖的影响，并检测瞠来瞬酸的IC55；将细胞随机分为w-NC组(转染阴性对照)、w - NC +d来e

酸组(转染阴性对照后，给予d来瞬酸处理)、W - VEGF组(转染si- VEGF)和-5 - VEGF + d来e酸组(转染

si- VEGF后,给予d来e酸处理)，TmusweX小室实验检测细胞的侵袭和迁移能力，Western blot检测细胞中

STAT3、p-STAT3和MMP-2蛋白的表达情况。结果:转染W-VEGF后成功下调BGC - 843细胞中VEGF

【收稿日期】2419 -92-4【基金项目】 河南省教育厅科研基金项目(编号：4B320093)【作者单位】I濮阳市安阳地区医院消化内科，河南安阳4557094郑州大学第二附属医院消化内科，河南郑州4570096河南大学第一附属医院消化内科，河南开封475009【作者简介】李自显(1979 -)，男，河南濮阳人，副主任医师，主要从事消化疾病临床与基础研究。E - mail：Uezimanpy@ 126. com 【通讯作者】杨文义(1974 -)，男，河南开封人，博士，副主任医师，主要从事消化内科工作。