Abstract:【Objective】 To research the effect and preliminary mechanism of integrin linked kinase.(ILK).on epithelial mesenchymal transition (EMT) in human glioma cells.【Methods】 The recombinant plasmid pEGFP–C1-ILK was successfully constructed and transfected into SHG-44 glioma cells and the stable transfected cell lines were selected by G418 previously by our project team. The experimental group is as follows: SHG-44 (mock group)

pEGFP-C1(empty vector group)

and pEGFP-C1-ILK (stable transition group). The expression of ILK and invasive ability were detected in every group at first. Then

the effect of overexpression of ILK on the EMT markers was tested. At last

by using the method of RNA silence and specific blockers BAY11-7028 separately

the NF-kB pathway was blocked. The expression of E-cadherin was detected by western blot to determine the effect of NF-kB pathway on the regulation of EMT in ILK-overexpressed cells. 【Results】 Overexpression of ILK

meanwhile

invasive ability enhancement(the result of transwell: number of cell migration in mock

empty vector and stable transfection group is 92

87

229)were found in the stable transfection group. Expression of EMT marker-protein was detected by western blot

and the expression of snail

slug

vimentin

twist in the stable transfection group was significantly higher than that in the control group and the empty vector group

while the expression of E-cadherin was significantly decreased in the stable transfection group

and the difference was statistically significant (P < 0.05). E-cadherin protein expression was significantly increased in the stable transfection group after BAY11-7028 and P65 SiRNA were used to block the pathway of NF-kB respectively. 【Conclusion】 Overexpression of ILK can make invasive ability enhanced

and down regulate E-cadherin

up regulate the expression of vimentin and Snail

Slug and Twist

which may promote the epithelial mesenchymal transition of glioma cells

and NF-kB pathway may participate in the process of regulation.