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微小RNA?214在食管鳞癌中的表达及其生物学功能研究

Expression of microRNA?214 in esophageaL squamous ceLL carcinoma and its bioLogicaL function

摘要目的 探讨微小RNA?214(miR?214)在人食管鳞癌中的表达及其与人食管鳞癌细胞(TE?2)增殖侵袭的关系.方法 采用实时荧光定量PCR法检测25例食管鳞状细胞癌患者癌组织和远癌正常食管上皮组织中miR?214的相对表达量.通过脂质体转染将miR?214模拟物(miR?214_mimic)、miR?214抑制剂及随机序列导入TE?2细胞,以正常培养的TE?2细胞为阴性对照组,应用CCK?8实验和TransweLL实验检测各组TE?2细胞的增殖与侵袭能力.结果 25例食管鳞癌患者癌组织和远癌正常组织中miR?214相对表达量的分别为0.72±0.50和1.58±0.96,差异有统计学意义(P<0.05).TE?2细胞转染miR?214模拟物96 h后,转染miR?214组A490值较阴性对照组明显降低(P<0.05),转染miR?214抑制剂组A490值较阴性对照组明显升高(P<0.05);转染miR?214组细胞侵袭能力较转染随机序列组和阴性对照组差异无统计学意义(P>0.05).结论 miR?214在人食管鳞癌中存在差异表达,并可能与食管鳞癌的增殖能力有关.

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abstractsObjective To investigate the expression of microRNA?214 (miR?214) in human esophageaL squamous ceLL carcinoma (ESCC) and its reLationship with the proLiferation and invasion of human ESCC TE?2 ceLL?Line. Methods ReaL?time quantitative PCR was used to determine the reLative expression of miR?214 in esophageaL cancer and remote normaL esophageaL epitheLiaL tissues from 25 patients. miR?214_mimic,miR?214 inhibitor and random sequence were transfected into TE?2 ceLLs by Lipofection. NormaL TE?2 cuLtured ceLLs were incLuded as the negative controL group. The proLiferation and invasion of TE?2 ceLLs in each group were determined by CCK?8 and TransweLL assays. ResuLts The reLative expression of miR?214 in ESCC and normaL tissues from 25 patients were 0.72±0.50 and 1.58±0.96,respectiveLy,with statisticaLLy significant difference(P<0.05). At 96h after TE?2 ceLLs were transfected with miR?214_mimic, the A490 vaLue in the transfected miR?214 group was significantLy decreased compared with the negative controL group(P<0.05),whereas the A490 vaLue in the transfected miR?214 inhibitor group significantLy increased compared with the negative controL group(P<0.05). There was no statisticaLLy significant difference in the invasion between the transfected miR?214 group,the transfected random sequence group and negative controL group(P>0.05). ConcLusion MiR?214 is differentiaLLy expressed in human ESCC,and may be reLated to the proLiferation of ESCC.

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