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作 者:傅寅佳[1] 杨熹[1] 曹小年[2] 来森艳[1] 王桂华[1] 胡俊波[1] 李襄[1]
机构地区:[1]华中科技大学同济医学院附属同济医院肿瘤研究所/胃肠外科,武汉430030 [2]华中科技大学同济医学院附属同济医院普胸外科,武汉430030
出 处:《华中科技大学学报(医学版)》2015年第3期247-250,共4页Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
基 金:国家自然科学基金资助项目(No.30973496);国家青年科学基金资助项目(No.81301899)
摘 要:目的探讨p55PIK对肝癌SMMC-7721细胞增殖能力的影响,及p55PIK上游可能的调控机制。方法以肝癌SMMC-7721细胞为研究对象,通过脂质体转染p55PIK特异性小干扰RNA(siRNA)si-p55构建p55PIK低表达的实验模型。通过CCK8检测p55PIK对肝癌SMMC-7721细胞增殖能力的影响。通过流式细胞术检测p55PIK对细胞周期进程的影响。转染针对p53的小干扰RNA(siRNA)si-p53低表达p53,采用Western blot检测p53对p55PIK表达的影响,并通过CCK8法检测p53对p55PIK在肝癌细胞增殖调控中的作用。结果低表达p55PIK可导致肝癌SMMC-7721细胞的增殖能力降低[转染后96h,si-NC组、si-p55组的A值分别为(1.325±0.050)、(1.183±0.019)],细胞周期G0/G1期阻滞[si-NC组:(39.07±2.02)%;si-p55组:(49.66±1.05)%]。低表达p53可在肝癌SMMC-7721细胞中上调p55PIK的表达。p55PIK可部分拮抗p53对肝癌SMMC-7721细胞增殖的抑制作用。结论p53可部分通过调控p55PIK抑制肝癌SMMC-7721细胞的增殖。Objective To examine the effects of p55 PIK on the proliferation of liver cancer cell line SMMC-7721 and the possible regulative mechanism of the upstream molecules of p55 PIK.Methods p55 PIK downexpression models were established by transfecting p55PIK-specific siRNA si-p55 into SMMC-7721 cells with lipofectamine.CCK8 assay was used to investigate the impact of p55 PIK on the proliferation of SMMC-7721 cells.The effect of p55 PIK on cell cycle was determined by flow cytometry(FCM).si-p53,a siRNA targeting p53,was used to detect the impact of p53 on the expression of p55 PIK by Western blot and on the proliferation of SMMC-7721 cells by using CCK8 assay.Results Knockdown of p55 PIK in liver cancer cell line SMMC-7721 inhibited the cell proliferation[96hafter transfection,A-value in si-NC and si-p55 were respectively(1.325±0.050)and(1.183±0.019)]and induced cell cycle arrest in G0/G1-phase[(39.07±2.02)%in si-NC and(49.66±1.05)%in si-p55].Low-expressing of p53 could up-regulate the expression of p55 PIK in SMMC-7721 cells.Knockdown of p55 PIK attenuated the impact of p53-knockdown on promoting the proliferation of SMMC-7721 cells.Conclusion p53 can inhibit the proliferation of liver cancer SMMC-7721 cells partially by down-regulating the expression of p55 PIK.
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