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  

Impact of ginkgo biloba extract on the malignant biological behavior of colon cancer cells by regulating CXCL12/CXCR4 signal pathway

作　　者：王玉杰 赵亚孟 吕振木 WANG Yu-jie;ZHAO Ya-meng;LYU Zhen-mu(Department of Gastroenterology,Hebei Hospital of Traditional Chinese Medicine,Shijiazhuang,Hebei 050000)

机构地区：[1]河北省中医院消化外科,河北石家庄050000

出　　处：《中国现代普通外科进展》2024年第4期270-274,共5页Chinese Journal of Current Advances in General Surgery

基　　金：河北省中医药管理局科研计划项目(2020095)。

摘　　要：目的:探讨银杏素(GK)调节趋化因子12(CXCL12)/趋化因子受体4(CXCR4)信号通路对结肠癌(CC)细胞恶性生物学行为的影响。方法:用不同浓度的GK(0、2.5、5、10μmol/L)处理结肠癌HCT116细胞48 h,MTT法检测HCT116细胞的存活率,筛选合适的GK浓度。将对数生长期的HCT116细胞分为对照组、GK组(5μmol/L GK)、CXCL12过表达重组腺病毒(Ad CXCL12)组、阴性对照(Ad NC)组、Ad CXCL12+CXCR4小干扰RNA(si CXCR4)组、Ad CXCL12+阴性对照(si NC)组。Transwell实验检测细胞迁移、侵袭;MTT及Tunel检测细胞增殖及凋亡变化;qRT-PCR及Western blot分别检测CXCL12、CXCR4 mRNA及蛋白表达水平。结果:5μmol/L GK处理细胞,其生存率最接近于50%,以此浓度进行后续研究。与对照组相比,GK组细胞增殖率、迁移、侵袭数与CXCL12、CXCR4 mRNA及蛋白表达水平显著降低,凋亡率显著增加(P<0.05);Ad CXCL12逆转了GK对HCT116细胞的抑制作用;si CXCR4逆转了Ad CXCL12对HCT116细胞的促进作用。结论:GK通过抑制CXCL12/CXCR4信号通路阻止HCT116细胞恶性生物学行为。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 receptor 4(CXCR4)signal pathway.Methods:Colon cancer HCT116 cells were treated with different concentrations of GK(0,2.5,5,10μmol/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(5μmol/L GK),CXCL12 overexpression recombinant adenovirus(Ad CXCL12)group,negative control(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 5μmol/L GK was the closest to 50%.Follow up studies were conducted at this concentration.Compared 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.

关 键 词：结肠肿瘤 银杏素 CXCL12/CXCR4信号通路 

分 类 号：R735.35[医药卫生—肿瘤]