Sam68基因对子宫内膜癌细胞增殖的影响  被引量:3

The effect of Sam68 gene on the proliferation of endometrial cancer cells

在线阅读下载全文

作  者:梁常艳[1] 杨越波[1] 李小毛[1] LIANG Chang-yan;YANG Yue-bo;LI Xiao-mao(Department of Gynecology,the Third Affiliated Hospital of Sun Yat-sen University,Guangzhou 510630,Guangdong,China)

机构地区:[1]中山大学附属第三医院妇科,广东广州510630

出  处:《广东医学》2020年第20期2064-2070,共7页Guangdong Medical Journal

基  金:广东省科技计划项目(2013B021800137)。

摘  要:目的探讨Sam68基因对人子宫内膜癌细胞增殖的影响.方法建立Sam68稳定干扰和过表达子宫内膜癌细胞株,Real-time PCR和Western blot验证干扰和过表达效率,MTT法、平板克隆法、软琼脂克隆形成实验、BrdU法检测沉默及过表达Sam68基因对子宫内膜癌细胞增殖活力的影响.结果利用逆转录病毒载体成功构建了Sam68 RNAi/HEC-1A、Sam68 RNAi/RL952以及Sam68 pc DNA-3/Ishikawa子宫内膜癌细胞模型.沉默Sam68基因可降低子宫内膜癌细胞增殖,抑制细胞的集落形成能力,而过表达则效果相反.结论利用RNAi靶向沉默Sam68基因可有效抑制人子宫内膜癌细胞的增殖,过表达则可促进增殖.Sam68在子宫内膜癌的发生发展中可能起到癌基因的作用.Objective To investigate the effect of Sam68 gene on the proliferation of human endometrial cancer cells. Methods To establish stable interference and overexpression of endometrial cancer cell lines of Sam68, and the efficiency was verified by real-time PCR and Western blot. The effects of Sam68 gene interfered or overexpressed on the proliferation of endometrial cancer cells was assessed by MTT, plate cloning, soft agar cloning and BrdU. Results Stable cell models of Sam68 RNAi/HEC-1 A, Sam68 RNAi/RL952 and Sam68 pc DNA-3/Ishikawa were successfully constructed with retrovirus vectors. Silencing Sam68 gene could reduce the proliferation of endometrial cancer cells and inhibit the colony forming ability of cells, while overexpression of Sam68 had the opposite effect. Conclusion Interfering with the expression of Sam68 gene by RNAi can effectively inhibit the proliferation of human endometrial cancer cells, while overexpression can promote the proliferation. Sam68 may play an oncogene role in development of endometrial cancer.

关 键 词:Sam68 子宫内膜癌 增殖 RNA干扰 过表达 

分 类 号:R737.33[医药卫生—肿瘤] R392.7[医药卫生—临床医学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象