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作 者:田鹤[1] 姜文丽[1] 楼国良[1] 黄才国[1] 陈若华[2]
机构地区:[1]第二军医大学附属长海医院儿科,上海200433 [2]第二军医大学附属长海医院特需诊疗科,200433
出 处:《临床肿瘤学杂志》2015年第6期487-491,共5页Chinese Clinical Oncology
基 金:国家自然科学基金面上项目(81473239)
摘 要:目的探讨醛酮还原酶家族1成员C1(AKR1C1)在非小细胞肺癌(NSCLC)组织和细胞株中的表达及其临床意义。方法采用免疫组化SP法检测50例NSCLC组织芯片中肿瘤及癌旁组织中AKR1C1的表达。选取NCI-H460细胞分别转染AKR1C1 si RNA(AKR1C1干扰组)和AKR1C阴性对照si RNA(阴性对照组)慢病毒载体,Western blotting验证转染效率,MTT法、低密度细胞集落形成实验、Transwell实验和划痕试验检测干扰AKR1C1表达对细胞增殖、集落形成、侵袭能力的影响,同时另设空白对照组(未转染慢病毒)。结果 NSCLC组织中AKR1C1的高表达率为94.0%(47/50),高于癌旁组织的6.0%(3/50),差异有统计学意义(P<0.05)。AKR1C1干扰组细胞中AKR1C1表达量较阴性对照组下调(P<0.05)。MTT法显示AKR1C1干扰组与阴性对照组细胞增殖率无显著性差异(P>0.05);AKR1C1干扰组、阴性对照组和空白对照组NCIH460细胞的克隆数分别为69.60±4.03、69.00±1.63和70.33±2.05,组间差异无统计学意义(P>0.05);Transwell实验显示,AKR1C1干扰组穿膜细胞数为15.30±2.50,低于阴性对照组的30.00±2.20和空白对照组的31.30±2.40,差异有统计学意义(P<0.05)。划痕试验显示,AKR1C1干扰组细胞迁移相对距离为0.13±0.05,低于阴性对照组的0.56±0.05和空白对照组的0.60±0.08,差异有统计学意义(P<0.05)。结论 AKR1C1在NSCLC组织中高表达,其可能与NSCLC转移相关。Objective To investigate the expression and clinical significance of AKR1C1 in nonsmall cell lung cancer ( NSCLC) tissues and cell line. Methods Immunohistochemical SP method was used to examine the expression of AKR1C1 in 50 cases of NSCLC tissues and matched adjacent normal tissues. NCIH460 cell was transfected with AKR1C1 siRNA( AKR1C1 interference group) and AKR1C1 negative control siRNA( negative control group) . Western blotting was used to confirm the results of transfection. The proliferation, colony formation and invasion ability were analyzed by MTT, lowdensity cell colony formation, woundinghealing and transwell experiments. The blank control group was set. Results The highlevel expression rates of AKR1C1 in cancer tissues were 94. 0%(47/50), which was higher than 6. 0%(3/50)in matched adjacent normal tissues (P〈0. 05). MTT analysis showed the proliferation rate of AKR1C1 interference group and negative control group was the same. The colony formation number of AKR1C1 interference group, negative control group and blank control group were 69. 60±4. 03, 69. 00±1. 63 and 70. 33±2. 05, with no significant difference. The number of migrated cells in AKR1C1 interference group was 15. 30±2. 50, which was lower than that of negative control group (30. 00±2. 20) and blank control group (31. 30±2. 40),with significant differences(P〈0. 05). The relative migrated distance of the cells in AKR1C1 interference group was 0. 13±0. 05, which was lower than that negative control group (0. 60±0. 08)and blank control group (0. 56±0. 05),with significant differences(P〈0. 05). Conclusion AKR1C1 is high expressed and may relate to the migration in NSCLC.
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