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DC-CIK诱导宫颈癌细胞休眠的实验研究

Experimental study of DC-CIK-induced cervical cancer cell dormancy
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摘要 目的分析树突状细胞(DC)-杀伤细胞(CIK)对宫颈癌细胞休眠的诱导作用。方法选取宫颈癌SiHa细胞,采集宫颈癌患者静脉血,经密度梯度离心法分离取得外周血单个核细胞层,分别诱导DC、CIK,分组培养后观察DC-CIK对宫颈癌SiHa细胞存活率及增殖、凋亡、侵袭、迁移等生物学行为的影响,Western blot法检测细胞凋亡、侵袭蛋白相对表达量。结果与宫颈癌组、DC组比较,CIK组、DC-CIK组增殖率较低,凋亡率较高;与CIK组比较,DC-CIK组增殖率较低,凋亡率较高(P<0.05)。与宫颈癌组、DC组比较,CIK组、DC-CIK组细胞存活率较低,且DC-CIK组存活率低于CIK组(P<0.05)。与宫颈癌组、DC组比较,CIK组、DC-CIK组侵袭、迁移细胞数较低;与CIK组比较,DC-CIK组侵袭、迁移细胞数较低(P<0.05)。与宫颈癌组、DC组比较,CIK组、DC-CIK组磷脂酰肌醇3-激酶(PI3K)、蛋白激酶B(AKT)、哺乳动物西罗莫司靶蛋白(mTOR)、基质金属蛋白酶-9(MMP-9)相对表达量较低,上皮性钙黏附素(E-cadherin)相对表达量较高;与CIK组比较,DC-CIK组PI3K、Akt、mTOR、MMP-9相对表达量较低,E-cadherin相对表达量较高(P<0.05)。结论建立DC-CIK共培养体系,并对宫颈癌细胞进行干预,能够抑制宫颈癌细胞增殖、侵袭、迁移,促进宫颈癌细胞凋亡,从而起到诱导宫颈癌细胞休眠的作用,其机制可能与使用DC-CIK细胞培养调控PI3K/Akt/mTOR通路蛋白及侵袭相关蛋白表达有关。 Objective To analyze the induction effect of dendritic cells(DC)-killeRcells(CIK)on cervical canceRcell dormancy.Methods Cervical canceRSiHa cells were selected,the venous blood of cervical canceRpatients with cervical canceRwas collected and peripheral blood mononucleaRcell layeRwas obtained from density gradient centrifugation,DC cells and CIK cells were induced respectively,the effects of DC-CIK cells on cervical canceRSiHa cells survival rate and proliferation,apoptosis,invasion,migration and otheRbiological behavioRwere observed afteRgroup culture,and Western blot method was used foRapoptosis and invasive protein expression.Results Compared with cervical canceRgroup and DC group,CIK group and DC-CIK group had loweRproliferation rate and higheRapoptosis rate.Compared with CIK group,the proliferation rate of DC-CIK group was loweRand the apoptosis rate was higheR(P<0.05).Compared with cervical canceRgroup and DC group,the survival rate of CIK group and DC-CIK group was lower,and the survival rate of DC-CIK group was loweRthan CIK group(P<0.05).Compared with cervical canceRgroup and DC group,the numbeRof invading and migrating cells in CIK group and DC-CIK group was lower.Compared with CIK group,the numbeRof invading and migrating cells in DC-CIK group was loweR(P<0.05).Compared with cervical canceRgroup and DC group,the relative expression levels of phosphatidylinositol 3-kinase(PI3K),protein kinase B(AKT),mammalian target of sirolimus(mTOR),matrix metalloproteinase-9(MMP-9)in CIK group and DC-CIK group were lower,and the relative expression levels of epithelial calcium adhesin(E-cadherin)were higher.Compared with CIK group,the relative expression levels of PI3K,Akt,mTORand MMP-9 were loweRin DC-CIK group,and the relative expression levels of E-cadherin were higheR(P<0.05).Conclusion The establishment of DC-CIK co-culture system and the intervention of cervical canceRcells can inhibit cervical canceRcell proliferation,invasion and migration,and promote cervical canceRcell apoptosis,thus inducing cervical canceRcell dormancy.The mechanism may be related to the use of DC-CIK cell culture to regulate PI3K/Akt/mTORpathway protein and invasion-related protein expression.
作者 赵晴 刘艳 邓渊润 Zhao Qing;Liu Yan;Deng Yuanrun(Dept of Obstetrics and Gynecology,The Third Affiliated Hospital of Southern Medical University,Guangzhou 510000)
出处 《安徽医科大学学报》 CAS 北大核心 2022年第10期1569-1573,共5页 Acta Universitatis Medicinalis Anhui
基金 国家自然科学基金(编号:82002743)。
关键词 宫颈癌 树突状细胞 杀伤细胞 细胞休眠 细胞存活率 cervical carcinoma dendritic cell killer cell cell dormancy cell viability
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