Title of article :
Knockdown of ZEB1, a master epithelial-to-mesenchymal transition (EMT) gene, suppresses anchorage-independent cell growth of lung cancer cells
Author/Authors :
Takeyama، نويسنده , , Yoshihiro and Sato، نويسنده , , Mitsuo and Horio، نويسنده , , Mihoko and Hase، نويسنده , , Tetsunari and Yoshida، نويسنده , , Kenya and Yokoyama، نويسنده , , Toshihiko and Nakashima، نويسنده , , Harunori and Hashimoto، نويسنده , , Naozumi and Sekido، نويسنده , , Yoshitaka and Gazdar، نويسنده , , Adi F. and Minna، نويسنده , , John D. and Kondo، نويسنده , , Masashi and Hasegawa، نويسنده , , Yoshinori، نويسنده ,
Abstract :
We found that among four master epithelial-to-mesenchymal transition (EMT)-inducing genes (ZEB1, SIP1, Snail, and Slug) ZEB1expression was most significantly correlated with the mesenchymal phenotype (high Vimentin and low E-cadherin expression) in non-small cell lung cancer (NSCLC) cell lines and tumors. Furthermore, ZEB1 knockdown with RNA interference in three NSCLC cell lines with high ZEB1 expression suppressed to varying degrees mass culture growth and liquid colony formation but in all cases dramatically suppressed soft agar colony formation. In addition, ZEB1 knockdown induced apoptosis in one of the three lines, indicating that the growth inhibitory effects of ZEB1 knockdown occurs in part through the activation of the apoptosis pathway. These results suggest that inhibiting ZEB1 function may be an attractive target for NSCLC therapeutic development.
Keywords :
MicroRNA , RNA interference , lung cancer , epidermal growth factor receptor , Anchorage-independent growth , EMT
