Impact of ginkgo biloba extract on the malignant biological behavior of colon cancer cells by regulating CXCL12/CX-CR4 signal pathway
10.3969/j.issn.1009-9905.2024.04.004
- VernacularTitle:银杏素调节CXCL12/CXCR4信号通路对结肠癌细胞恶性生物学行为的影响
- Author:
Yu-Jie WANG
1
;
Ya-Meng ZHAO
;
Zhen-Mu LYU
Author Information
1. 河北省中医院 消化外科(河北 石家庄 050000)
- Keywords:
Colon neoplasms;
Ginkgo biloba extract;
CXCL12/CXCR4 signal pathway
- From:
Chinese Journal of Current Advances in General Surgery
2024;27(4):270-274
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the impact of ginkgo biloba extract(GK)on the malignant biological behavior of colon cancer(CC)cells by regulating the chemokine 12(CXCL12)/chemokine re-ceptor 4(CXCR4)signal pathway.Methods:Colon cancer HCT116 cells were treated with different concentrations of GK(0,2.5,5,10 μ mol/L)for 48 hours,MTT assay was used to detect the survival rate of HCT116 cells and screen the appropriate GK concentration.HCT116 cells in logarithmic growth phase were divided into control group,GK group(5 μ mol/L GK),CXCL12 overexpression re-combinant adenovirus(Ad CXCL12)group,negative controI(Ad NC)group,Ad CXCL12+CXCR4 small interfering RNA(si CXCR4)group,and Ad CXCL12+negative control(si NC)group.Transwell assay was used to detect cell migration and invasion;MTT and Tunel were used to detect cell proliferation and apoptosis;and the mRNA and protein expression levels of CXCL12 and CXCR4 were detected by qRT PCR and Western blot respectively.Results:The survival rate of cells treated with 5μ mol/L GK was the closest to 50％.Follow up studies were conducted at this concentration.Com-pared with the control group,the cell proliferation rate,migration,invasion numbers,the expression levels of CXCL12,CXCR4 mRNA and protein in GK group decreased obviously,and the apoptosis rate increased obviously(P＜0.05);Ad CXCL12 reversed the inhibitory effect of GK on HCT116 cells.si CXCR4 reversed the promoting effect of Ad CXCL12 on HCT116 cells.Conclusion:GK inhibits the malignant biological behavior of HCT116 cells by inhibiting CXCL12/CXCR4 signaling pathway.
