局解手术学杂志2024，Vol.33Issue(5)：388-393,6.DOI:10.11659/jjssx.03E023052
青蒿素抑制葡萄糖刺激下结直肠癌细胞恶性生物学行为的机制研究
Mechanism of artemisinin inhibiting malignant biological behavior of colorectal cancer cells stimulated by glucose
摘要
Abstract
Objective To investigate the effect of artemisinin(ART)on the malignant biological behavior of colorectal cancer(CRC)cells stimulated by glucose and its mechanism.Methods The concentration gradients of 0,5,10,20,40 and 60 μmol/L of ART were used to treat the human colorectal cancer cell line SW480,and then the cell viability was detected by CCK-8.Cell apoptosis was detected by flow cytometry.Transwell was used to detect the cell migration and invasion.Western blot was used to detect the apoptosis,epithelial-mesenchymal transition(EMT)and Janus kinase 2(JAK2)/signal transducer and activator of transcription 3(STAT3)related proteins expression.Results Compared with the 0 μmol/L of ART,the viability of SW480 cells decreased under 5,10,20,40,60 μmol/L of ART treatment(P<0.05),and IC50 was 36.91 μmol/L.Therefore,the cells treated with 10,20 and 40 μmol/L of ART were as the low-dose,medium-dose and high-dose ART groups,the cells treated with 0 μmol/L of ART were as the control group,and the cells treated with 40 μmol/L of ART and 10 μmol/L of Coumermycin A1 were as the Coumermycin A1 group.Compared with the control group,the cell scratch wound healing rate,invasion ability,and expression levels of Bcl-2,N-cadherin,Vimentin,p-JAK2,and p-STAT3 in the low-dose ART group,the medium-dose ART group,and the high-dose ART group decreased obviously(P<0.05),while the apoptosis rate,and expression levels of Bax,Caspase-3 and E-cadherin increased(P<0.05).Compared with the high-dose ART group,the cell scratch wound healing rate,invasion ability,and expression levels of Bcl-2,N-cadherin,Vimentin,p-JAK2,and p-STAT3 in the Coumermycin A1 group increased obviously(P<0.05),while the apoptosis rate,and expression levels of Bax,Caspase-3 and E-cadherin decreased(P<0.05).Conclusion ART may inhibit the viability,migration,invasion and EMT of glucose-stimulated CRC cells and promote apoptosis by inhibiting the JAK2/STAT3 signaling pathway.关键词
青蒿素/结直肠癌/恶性生物学行为/Janus激酶2/信号转导与转录激活因子3Key words
artemisinin/colorectal cancer/malignant biological behavior/Janus kinase 2/signal transducer and activator of transcription 3分类
医药卫生引用本文复制引用
潘勇娜,常月锋,郭璟静,孙依礼,魏岚,杨春雁,康金旺..青蒿素抑制葡萄糖刺激下结直肠癌细胞恶性生物学行为的机制研究[J].局解手术学杂志,2024,33(5):388-393,6.基金项目
河北省卫生健康委项目资助(20210473) （20210473）
