Effect of Ginsenoside Rh2 on Metastasis and Invasion of Colorectal Cancer Resistant Cells HCT116/L-OHP and Its Mechanism
10.13422/j.cnki.syfjx.20191324
- VernacularTitle: 人参皂苷Rh2对结肠癌耐药细胞HCT116/L-OHP侵袭迁移能力的影响
- Author:
Ke-min YAN
1
;
Hai-juan XIAO
2
;
Lin YANG
3
;
Jiao-jiao WANG
1
;
Jia SUN
1
;
Shuang-shuang HU
4
;
Meng GUO
2
;
Yong-zhan NIE
2
;
Dai-ming FAN
2
Author Information
1. Shaanxi University of Chinese Medicine, Xianyang 712046, China
2. Xijing Hospital of Digestive Disease, Air Force Medical University, Xi'an 710032, China
3. Xianyang Central Hospital, Xianyang 712000, China
4. Hospital Affiliated to Shaanxi University of Chinese Medicine, Xianyang 712000, China
- Publication Type:Research Article
- Keywords:
GRh2;
colon cancer resistant cells HCT116/L-OHP;
invasion;
migration;
E-cadherin;
matrix metalloproteinase-9(MMP-9)
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2019;25(13):73-78
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To observe effect of ginsenoside Rh2 (GRh2) on the invasion and migration of colon cancer resistant cells HCT116/L-OHP and its specific mechanism. Method:Cell counting kit-8 (CCK-8) assay was used to detect the inhibitory effect of different concentrations of GRh2 (0, 2.5, 5, 10, 20, 40 mg·L-1) on HCT116/L-OHP cell proliferation, scratch assay, Transwell assay and adhesion assay were used to detect the effects of GRh2 (0, 2.5, 5, 10 mg·L-1) on cell migration, invasion and adhesion. The protein expression levels of E-cadherin and matrix metalloproteinase-9(MMP-9) were examined by Western blot. Result:Compared with control group, GRh2(5, 10, 20, 40 mg·L-1) significantly inhibited the proliferation of HCT116/L-OHP cells in a dose-dependent manner(P<0.05, P<0.01); Compared with the control group, the scratch healing rate of GRh2 group (5, 10 mg·L-1) was significantly decreased (P<0.05, P<0.01), the number of cells passing through the chamber of GRh2 group was significantly decreased (P<0.05, P<0.01), cell migration and invasive ability were significantly inhibited in a dose-dependent manner. The number of adherent cells in GRh2 group was significantly reduced (P<0.05, P<0.01), and the cell adhesion ability was significantly inhibited. Compared with the control group, GRh2 (10, 20, 30 mg·L-1) promoted E-cadherin protein expression (P<0.05, P<0.01), while protein expression of MMP-9 was inhibited (P<0.01). Conclusion:GRh2 can significantly inhibit the invasion and migration of HCT116/L-OHP in colon cancer cells, and its potential mechanism may be related to the promotion of E-cadherin and the inhibition of MMP-9 expression in a dose-dependent manner.
