Knockdown of KIF3C Inhibits Epithelial-Mesenchymal Transition in Lung Cancer Cells A549

The objective of this study is to reveal the role of KIF3C gene in the proliferation of lung cancer cells,and the regulation of epithelial mesenchymal transition(EMT)of tumor cells.The plate clone formation assay and cell scratch assay were used in this study to detect the changes of cell proliferation and migration ability after siKIF3C interference,while EMT-related protein expression after KIF3C downregulation was detected by Western blot.The cell clone formation assay showed that the number of clones of lung cancer cells A549 was significantly reduced after transfected with siKIF3C(P<0.05);The scratch assay showed that the healing ability of cells was significantly reduced after transfected with siKIF3C(P<0.05);Western blot protein analysis revealed that the levels of EMT-related proteins,N-cadherin,Vimentin,Snail,and Slug were significantly down-regulated(P<0.05),however,E-cadherin protein levels were up-regulated after siKIF3C interference.In conclusion,KIF3C may promote the proliferation and invasive ability of lung cancer cells A549 through EMT.

KIF3C Promotes the Malignant Progression of Lung Cancer Cells A549

Objective:To investigate the role of KIF3C gene in promoting the malignant phenotype of lung cancer cells and in regulating PI3K/AKT signaling pathway.Methods:CCK-8 and transwell assays were used to detect the changes in cell proliferation and cell migration ability after being transfected with siKIF3C,as well as the protein expression levels of PI3K,p-PI3K,AKT,and p-AKT following the downregulation of KIF3C by Western blot.Results:The CCK-8 assay showed that the proliferation/viability of lung cancer cells A549 significantly reduced after being transfected with siKIF3C gene(P<0.05);the migration ability of lung cancer cells A549 was significantly reduced after transfected with siKIF3C gene(P<0.05);the levels of p-PI3K and p-AKT proteins were downregulated after KIF3C protein knockdown(P<0.05);however,the detection of PI3K and AKT protein levels was not statistically significant.Conclusion:KIF3C may promote the proliferation and migration ability of lung cancer cells A549 through PI3K/AKT signaling pathway.