Experimental study on the inhibition effect of miR-106a inhibitor on tumor growth of ovarian cancer xenografts mice
10.1016/j.apjtm.2016.05.008
- Author:
Zhi-Hui CAI
1
;
Li-Min CHEN
1
;
Yi-Juan LIANG
1
;
Jun-Rong SHI
1
;
Jun-Rong YOU-JU
1
;
Wei-Ming WANG
1
;
Huan YANG
2
Author Information
1. Gynecology Department, Affiliated Hospital of Hebei University
2. Gynecology and Obstetrics Department, Jingxiu District Hospital of Baoding City
- Publication Type:Journal Article
- Keywords:
miR-106a;
Ovarian cancer;
Programmed cell death 4;
Xenografts
- From:
Asian Pacific Journal of Tropical Medicine
2016;9(7):698-701
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the inhibition effect of miR-106a inhibitor on tumor growth of ovarian cancer xenografts mice. Methods BALB/c mice were selected as experimental animals, ovarian cancer SKOV-3 cells transfected with miR-106a inhibitor and its negative control were inoculated subcutaneously, intratumoral injection of miR-106a inhibitor and its negative control were continued after tumor formation, and they were enrolled as treatment group and model group, respectively. Tumor volume and weight as well as Ki-67 and programmed cell death 4 (PDCD4) expression were determined; miR-106a inhibitor and its negative control as well as miR-106a mimic and its negative control were transfected into SKOV-3 cells, and expression of PDCD4 in cells was determined. Results Tumor tissue volume and weight as well as mRNA expression and protein expression of Ki-67 in treatment group were significantly lower than those in the model group while mRNA expression and protein expression of PDCD4 were significantly higher than those in the model group; transfection of miR-106a mimic could decrease mRNA expression and protein expression of PDCD4 in SKOV-3 cells, and transfection of miR-106a inhibitor could increase mRNA expression and protein expression of PDCD4 in SKOV-3 cells. Conclusions Transfection of miR-106a inhibitor can inhibit the growth of tumor in ovarian cancer xenografts mice through increasing the expression of PDCD4.
