Effect of Xianlian Jiedu Prescription on Proliferation and Glycolysis of Human Colorectal Cancer HCT-116 Cells and Mechanism
10.13422/j.cnki.syfjx.20220729
- VernacularTitle:仙连解毒方对人结直肠癌细胞增殖及糖酵解的调控作用及机制
- Author:
Li-huiping TAO
1
;
Yue-yang LAI
2
;
Hai-bo CHENG
1
;
Wei-xing SHEN
1
;
Jia-ni TAN
1
;
Chang-liang XU
1
;
Cheng-tao YU
1
;
Min-min FAN
1
;
Liu LI
1
;
Zheng-jie SHEN
3
Author Information
1. The First Clinical College，Nanjing University of Chinese Medicine， Nanjing 210023， China
2. Jiangsu Collaborative Innovation Center of Traditional Chinese Medicine in Prevention and Treatment of Tumor， Nanjing 210023， China
3. Zhangjiagang Hospital Affiliated to Soochow University， Suzhou 215600，China
- Publication Type:Journal Article
- Keywords:
colorectal cancer;
Xiaolian Jiedu prescription;
glycolysis;
proliferation
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2022;28(8):72-78
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo explore the effect of Xianlian Jiedu prescription （XLJDP） on the proliferation and glycolysis of human colorectal cancer HCT-116 cells and the underlying mechanism. MethodHCT-116 cells were cultured with XLJDP and then the survival rate was examined by methyl thiazolyl tetrazolium （MTT） assay. The effect on the HCT116 cell proliferation was detected by colony formation assay and 5-ethynyl-2′-deoxyuridine （EDU） incorporation assay. The amount of glucose consumed by HCT-116 cells was measured by glucose test kit， and the amount of produced lactic acid was determined by lactic acid test kit 48 h after the treatment with XLJDP. The expression of glycolysis-related proteins mammalian target of rapamycin （mTOR）， phosphorylated mTOR （p-mTOR）， glucose transporter 1 （GLUT1）， and lactate dehydrogenase （LDHA） was detected by Western blot. ResultThe half-maximal inhibitory concentration （IC50） of XLJDP against HCT-116 cells was 6.82 g·L-1. Compared with the blank group， XLJDP （1.625， 3.25， 6.50 g·L-1） inhibited the proliferation of HCT-116 cells （P<0.05， P<0.01）. Moreover， compared with the blank group， XLJDP （1.625， 3.25， 6.50 g·L-1） suppressed glucose uptake and lactic acid production in a dose-dependent manner （P<0.05， P<0.01）. The expression of p-mTOR/mTOR， LDHA， and GLUT1 was down-regulated by XLJDP （P<0.05， P<0.01）. ConclusionXLJDP can significantly inhibit the proliferation and the Warburg effect of glycolysis in colorectal cancer cells by regulating the mTOR signaling pathway and the down-regulating the expression of LDHA， GLUT1， and other key proteins and enzymes in glycolysis.
