首页|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

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

扫码查看
目的 探讨青蒿素(ART)对葡萄糖刺激下结直肠癌(CRC)细胞的恶性生物学行为的影响及其作用机制.方法 以0、5、10、20、40、60 μmol/L ART为浓度梯度处理人结直肠癌细胞株SW480,然后采用CCK-8法检测细胞活力.流式细胞术检测细胞凋亡情况;Transwell检测细胞迁移和侵袭情况;Western blot检测细胞凋亡、上皮-间质转化(EMT)及Janus激酶2(JAK2)/信号转导与转录激活因子3(STAT3)相关蛋白表达.结果 与0 μmol/L ART相比,5、10、20、40、60 μmol/L ART处理下SW480细胞活力降低(P<0.05),IC50为36.91 μmol/L.故以10、20、40 μmol/L ART处理的细胞为ART低、中、高剂量组,以0 μmol/L ART处理的细胞为对照组,以ART 40 μmol/L+Coumermycin A1 10 μmol/L处理的细胞为Coumermycin A1组.与对照组相比,ART低剂量组、ART中剂量组、ART高剂量组细胞划痕愈合率、侵袭能力及Bcl-2、N-cadherin、Vimentin、p-JAK2、p-STAT3表达显著下降(P<0.05),细胞凋亡率及Bax、Caspase-3、E-cadherin表达上升(P<0.05);与ART高剂量组相比,Coumermycin A1组细胞划痕愈合率、侵袭能力及Bcl-2、N-cadherin、Vimentin、p-JAK2、p-STAT3 表达水平显著上升(P<0.05),细胞凋亡率及Bax、Caspase-3、E-cadherin表达水平下降(P<0.05).结论 ART可能通过抑制JAK2/STAT3信号通路,抑制葡萄糖刺激下CRC细胞活力、迁移、侵袭和EMT,促进其凋亡.
Mechanism of artemisinin inhibiting malignant biological behavior of colorectal cancer cells stimulated by glucose
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.

artemisinincolorectal cancermalignant biological behaviorJanus kinase 2/signal transducer and activator of transcription 3

潘勇娜、常月锋、郭璟静、孙依礼、魏岚、杨春雁、康金旺

展开 >

河北北方学院附属第二医院消化内科,河北 张家口 075100

河北北方学院基础医学院,河北 张家口 075000

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3

河北省卫生健康委项目资助

20210473

2024

局解手术学杂志
重庆市解剖学会,第三军医大学

局解手术学杂志

CSTPCD
影响因子:1.063
ISSN:1672-5042
年,卷(期):2024.33(5)
  • 20