MICAL-L2 Promotes Migration And Proliferation Of Colorectal Cancer Cells By Activating AKT/β-catenin Signal Pathway

PurposeTo investigate the role of MICAL-L2 in colorectal cancer cells and analyze its potential molecular mechanisms.MethodsFirst,the expression level of MICAL-L2 in colorectal cancer tissues were assessed by q-PCR and immunohistochemical staining assay,and analyze the relationship between MICAL-L2 expression level and clinicopathological parameters of patients with colorectal cancer.The effects of MICAL-L2 on the migration,proliferation of colorectal cancer cells were detected by wound healing assay and soft agar clony formation assay.And the effect of MICAL-L2 on the proliferation of colorectal cancer cells was detected by xenografts tumor experiments.Finally,to explore the molecular mechanism of MICAL-L2 in colorectal cancer cells,the molecules levels of AKT/β-catenin signaling pathway were detected by Western blot method.ResultsThe results of q-PCR and immunohistochemical staining showed that the expression level of MICAL-L2 in colorectal cancer tissues was significantly higher than that of adjacent tissues,and the expression level of MICAL-L2 was positively correlated with lymph node metastasis.in vitro experiments confirmed that MICAL-L2 significantly promotes the migration of colorectal cancer cells and the proliferation of colorectal cancer cells.the results of nude mice tumor-bearing experiments also found that the expression of MICAL-L2 significantly promotes the growth of colorectal cancer cells;the results from Western blot showed that overexpression of MICAL-L2 increased the protein level and nuclear translocation of β-catenin,while reducing the phosphorylation level of β-catenin.In addition,overexpression of MICAL-L2 increased the phosphorylation level of AKT,while PI3 K inhibitor(LY294002)can block the the effects caused by the overexpression of MICAL-L2.ConclusionsThe up-regulated MICAL-L2 in colorectal cancer can induce EMT to promote the migration of colorectal cancer cells;MICAL-L2 promotes the proliferation of colorectal cancer cells,which may be mediated by activating the AKT/β-catenin signaling pathway.