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Objective: To study Sphk1 on colon cancer Lovo cell proliferation, apoptosis and invasion and to explore its mechanism . Methods: A human colon cancer cell line Lovo experimental model were divided into Sphk1 activation group (PMA group ), Sphk1 suppression group (DMS group ) , control group (Normal group ) . With Phorbol 12-myristate 13-acetate (PMA) was Sphk1 activator ( final concentration of 100nM), Erythro-sphingosine, N, N-Dimethyl (DMS) is Sphk1 inhibitor ( final concentration of 50μM) Lovo cells for 24 hours after treatment , determined by MTT cell proliferation activity , cell apoptosis was detected by flow cytometry using Transwell invasion assay cell invasion , determined by Western blot cell Sphk1, ERK1 / 2, p-ERK1 / 2, NF-κB p65 protein levels . Results : PMA can induce protein expression Sphk1 Lovo cells and promote cell growth and inhibit apoptosis and promote cell invasion ; contrary , DMS inhibited the expression of Sphk1 inhibit cell growth promoting cell apoptosis and inhibition of cell invasion (0.28 ± 0.017 VS 0.19 ± 0.031,1.11 ± 0.19 VS 0.28 ± 0.17,9.15% VS 32.58%, 190.57% VS 9.65%). PMA-induced Sphk1 expression , accompanied by ERK1 / 2, p-ERK1 / 2 and NF-κB p65 protein upregulation , DMS inhibited Sphk1 expression inhibited ERK1 / 2, p-ERK1 / 2, NF-κB p65 protein expression (0.28 ± 0.017 VS 0.19 ± 0.031,0.64 ± 0.054 VS 0.42 ± 0.035,0.69 ± 0.076 VS 0.37 ± 0.018,0.29 ± 0.019VS 0.17 ± 0.026). Conclusion : Sphk1 Lovo cells can promote the growth inhibition of cell proliferation and invasion and apoptosis , which may be related ERK1 / 2 and NF-κB signaling pathway activation.
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