Effect of resolvin D1 on the crosstalk of K-Ras/Notch signaling of colon cancer cells
Objective To investigate the effect of resolvin D1(RvD1)on K-Ras/Notch signaling in SW620 colon cancer cells and its mechanism.Methods The effects of RvD1(0.0,62.5,125.0,250.0,500.0 nmol/L)on the short and long term proliferation of SW620 colon cancer cells were evaluated by CCK-8 and clonal formation methods.SW620 colon cancer cells were divided into blank group,RvD1 group,K-Ras group and K-Ras+RvD1 group.Blank group was not treated,K-Ras group and K-Ras+RvD1 group were transfected with K-Ras plasmid,and RvD1 group and K-Ras+RvD1 group were treated with 250 nmol/L RvD1.The expressions of IL-6,K-Ras,NICD,p-p65,p65,vimentin,N-cadherin,and E-cadherin were detected by Western blot.The expressions of IL-6,K-Ras,and NICD were detected by immunofluorescence.The levels of cell invasion and migration were detected by Transwell assay.Results 125.0,250.0,500.0 nmol/L RvD1 inhibited the proliferation and clonal formation of SW620 cells(P＜0.05).The expression of IL-6,K-Ras,NICD,P-P65,vimentin,and N-cadherin in RvD1 group were lower than those in blank group,while the expression of E-cadherin was higher than that in blank group,with statistical significances(P＜0.05).The protein expressions of NICD,P-P65,vimentin,and N-cadherin in K-Ras group were higher than those in blank group,and the expression of E-cadherin was lower than that in blank group,with statistical significances(P＜0.05).The expression levels of NICD,P-P65,vimentin,and N-cadherin in K-Ras+RvD1 group were lower than those in K-Ras group,and the expression levels of E-cadherin were higher than those in K-Ras group,with statistical significances(P＜0.05).Conclusion By inhibiting the expression of IL-6,inhibiting K-Ras cross-talk to Notch signaling pathway,decreasing the downstream nuclear factor-κB level and epithelial-mesenchymal transformation,RvD1 can weaken the invasion and metastasis of colon cancer cells.
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