Experimental study on the inhibition effect of miR-106a inhibitor on tumor growth of ovarian cancer xenografts mice
Experimental study on the inhibition effect of miR-106a inhibitor on tumor growth of ovarian cancer xenografts mice作者机构：Gynecology DepartmentAffiliated Hospital of Hebei University Gynecology and Obstetrics DepartmentJingxiu district hospital of Baoding city
出 版 物：《Asian Pacific Journal of Tropical Medicine》 (亚太热带医药杂志（英文版）)
年 卷 期：2016年第9卷第7期
页 面：663-666页
核心收录：
学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学]
基 金：supported by Science and Technology Program of Hebei Province in 2013 (No.132777163)
主 题：Ovarian cancer Xenografts miR-106a Programmed cell death 4
摘 要：Objective:To study the inhibition effect of miR-106 a inhibitor on tumor growth of ovarian cancer xenografts ***:BALB/c mice were selected as experimental animals,ovarian cancer SKOV-3 cells transfected with miR-106 a inhibitor and its negative control were inoculated subcutaneously,intratumoral injection of miR-106 a inhibitor and its negative control were continued after tumor formation,and they were enrolled as treatment group and model group,*** volume and weight as well as Ki-67 and programmed cell death 4(PDCD4) expression were determined;miR-106 a inhibitor and its negative control as well as miR-106 a mimic and its negative control were transfected into SKOV-3 cells,and expression of PDCD4 in cells was ***:Tumor tissue volume and weight as well as mR NA expression and protein expression of Ki-67 in treatment group were significantly lower than those in the model group while m RNA expression and protein expression of PDCD4 were significantly higher than those in the model group;transfection of mi R-106 a mimic could decrease m RNA expression and protein expression of PDCD4 in SKOV-3 cells,and transfection of miR-106 a inhibitor could increase mR NA expression and protein expression of PDCD4 in SKOV-3 ***:Transfection of mi R-106 a inhibitor can inhibit the growth of tumor in ovarian cancer xenografts mice through increasing the expression of PDCD4.
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