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岭南现代临床外科 ›› 2017, Vol. 17 ›› Issue (03): 261-266.DOI: 10.3969/j.issn.1009-976X.2017.03.002

• 论著与临床研究 • 上一篇    下一篇

miRNA?135a在肝癌组织中的表达及临床意义

李文宏 曾宪成 王捷   

  1. 广州市增城区人民医院(中山大学附属博济医院)
  • 通讯作者: 王捷
  • 基金资助:

    2014年广州市医药卫生科技一般引导项目;广州市卫生局项目;广州市卫生局项目

Expression of miRNA-135a in the Hepatic carcinoma and its clinical significance

LI Wenhong, ZENG Xiancheng, WANG Jie   

  • Online:2017-06-20 Published:2017-06-20
  • Contact: WANG Jie

摘要:

 目的 miRNA?135amiR?135a在肝癌组织中的表达及其临床意义。方法 用实时荧光定PCR20例肝癌组织及其癌旁组织miR?135a的表达水, 并通过脂质体导的方法miR?135a模拟miR?135amimics转染肝癌细胞HepG2采用实时荧光定PCR定转染后细胞miR?135a的表达水平通过平板克隆实验MTT法分别检测转染后细克隆成率和存活率的变miR?135a调控相关靶细胞的基因表达水平进行检miR?135a肝癌细胞维持正常功能中的作结果 通过20例肝癌组织及其癌旁组织miR?135a的表水平进行检测miRNA?135a的表达在正常组织中相对更高且两组之间存在显著性差P<0.05与阴性对照组比较转染miR?135amimicsHepG2细胞中miR?135a表达水平显著提P<0.05而形成单克隆能力和细胞存活率均显著下P<0.05同时转细胞中miR?135a细胞调控相关靶基因FOSPI3Jak2Stat3mRNA表达量相较NC组均显著降P<0.05,表明miR?135a表达提高后抑制细胞形成单克隆能力并降低存活结论 miR?135a在正常织和肝癌组织中差异表达同时miR?135a表达提高时抑制肝癌细胞形成单克隆能力和降低细存活率miR?135a可能通过一些相关靶基因直接或间接调HepG2肝癌细胞的存活在肝的发生过程中可能起到作用miR?135a可能成为临床治疗肝癌和预后的重要靶

关键词: HepG2 细胞, 肝癌, miR?135a, miR?135a mimics

Abstract:

Objective To explore the expression of miRNA-135amiR-135ain the hepatic carcinoma and its clinical significance. Methods The level of expression of miR-135a in the hepatic carcinoma tissues of 20 patients with hepatic carcinoma and the commensurate adjacent normal liver tissues were detected by real?time quantitation PCR. HepG2 cells were transfected with miR?135a mimics mediated by liposomal transfection reagent and the expression of miR-135a in the transfected HepG2 cells were detected by real?time quantitation PCR. The changes of cell clone formation rat and cell viability were analyzed by tablet clone formation experimentPCFand MTT method, respectively. Meanwhile, the expression of the related genes of miR?135a regulation were analyzed to discover the role of miR?135a in maintain normal function. Results The miR-135a was detected in both hepatic carcinoma and commensurate adjacent normal liver tissues. The expression of miR-135a in the commensurate adjacent normal liver tissues were significantly higher than that in the hepatic carcinoma P<0.05. Compared with negative control, the expression of miR-135a in the miR?135a mimics transfected HepG2 cells was significantly increased P<0.05, however, the clone formation rate and viability were significantly decreased P<0.05. And the expression of miR-135a regulation related genes including FOS, PI3, Jak2, Stat3 were all down regulatedP<0.05. These data suggested that the up?regulated of miR-135a could inhibited the clone formation rate and decrease the cell viability. Conclusion miR-135a was differently expression in hepatic carcinoma and normal liver tissues and the up-regulated of miR-135a could inhibited the clone formation rate and decrease the cell viability. miR-135a contributed to the viability and occurrence of hepatic carcinoma by regulated of the related genes directly or indirectly, miR?135a may became the important target for clinical treatment and prognosis of hepatic carcinoma.

Key words: miR?135a, HepG2, Hepatic carcinoma, miR?135a mimics

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