The Research Of The Inhibition Of Invasion And Metastasis Of Colon Cancer Cells HCT116after Administrate YiQiFuShengFang By ERK/MAPK Signaling Pathway

Objective:To research the interaction mechanisms of anti-invasion and metasta-sis of tumor after using YiQiFuShengFang on HCT116though Mitogen acttiveatedprotein Kinase/Extracellular signal-regulated kinase signal pathway,providing somebasis of scientific experiments of anti-invasion and metastasis of tumor in using Tr-aditional Chinese Medical prescription. Methods:The proliferation of colon cancercells HCT116was observed by methylthiazolyl tetrazoliym(MTT) assay. Selecting t-he appropriate drug density to carry on the next step of the experiment.The effectof the migration of HCT116cells that treated by YiQiFuShengFang was examinedby Scratch test. ELISA method was adopted to test the express of Vascular endoth-elial growth factor(VEGF) on HCT116cells after administrated medicine.ELISA m-ethod was adopted to test the express of Matrix Metalloproteinase-2(MMP-2) on H-CT116cells after administrated drugs. The cell cycle and apoptosis of HCT116ce-lls that conducted by YiQiFuShengFang were examined by Flow Cytometry(FCM).p-ERK1/2expression was determined by Western-blot, in that was the activation ofERK1/2which was measured by the extent of ERK phosphorylation.Results: MTTassay showed the proliferation of colon cancer cells HCT116could be inhibited b-y YiQiFuShengFang. YiQiFuShengFang inhibited the migration of HCT116cells. Y-iQiFuShengFang reduced the expressing of VEGF,meanwhile,it cut down the expre-ssing of MMP-2. Through the analysis of flow cytometric, the apoptosis of tumorcells were significantly higher and cell cycle was changed. Western blot assay sho- wed that ERK1/2phosphorylation was suppressed by YiQiFuShengFang,that is ERK1/2could be inactivated by the downregulation of p-ERK1/2.Coclusion:YiQiFuShen-gFang inhibits the proliferation of colon cancer cells HCT116，down-regulates the expression of VEGF and MMP-2,and induces the apoptosis of cancer cells which may be mediated by ERK/MAPK signaling pathway.