1. Low expression S100 calcium ion binding protein A6 promoting the proliferation and migration of esophageal adenocarcinoma SK-GT-4 cells
Ke-Ke HUANG ; Bo QI ; Cheng-Wei CU ; Shu-Hua HUO ; Yu-Zhen UIU ; Bao-Sheng ZHAO ; Ke-Ke HUANG ; Bo QI ; Cheng-Wei CU ; Shu-Hua HUO ; Yu-Zhen UIU ; Bao-Sheng ZHAO ; Ke-Ke HUANG ; Yu-Zhen UIU
Acta Anatomica Sinica 2021;52(5):737-743
Objective To explore the effect of S100 calcium ion binding protein A6 (S100A6) on proliferation and migration of esophageal adenocarcinoma SK-GT-4 cells. Methods Lenti viruses were used to construct stable transfected cell lines (shNC and shS100A6). Real-time PCR was used to detect the mRNA expression of S100A6. The inverted microscope and MTT were used to detect cell proliferation. The Transwell assay was used to detect cell migration. Western blotting was used to detect the expression of S100A6, p-ERK, p-Akt and its downstream molecular involved in proliferation and migration. Using U0126 ( inhibitor of MER1/2) and LY294002 ( inhibitor of PI3K) to detect the effect of these two inhibitors on cell proliferation and migration and the expression of p-ERK, p-Akt and its downstream molecular involved in proliferation and migration in shS100A6 cells. Results Stable cell lines of knockdown S100A6 were constructed. Knockdown S100A6 promoted cell proliferation and migration. Western blotting result displayed that in shS100A6 cells, the levels of p-Akt and p-ERK increased, p21 decreased, cyclinDl increased, and the expression of β-catenin and vimentin, increased. U0126 and LY294002 inhibited the migration of shS100A6 cells. U0126 had no effect on the proliferation of shS100A6 cells, however LY294002 could inhibit the proliferation of shS100A6 cells. U0126 treatment on shS100A6 cells could decrease p-ERK and β-catenin expression. After shS100A6 cells treated with LY294002, p-Akt and β-catenin expression decreased, p21 expression increased and the expression of cyclinDl decreased. Conclusion Low expression of S100A6 promotes cell proliferation and migration, which may be mediated by activation of p-Akt regulating cell cycle progression to promote cell proliferation and by activation of p-Akt/p-ERK to regulate β-catenin to promote cell migration.
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