Author/Authors :
Obara، نويسنده , , Soichi and Nakata، نويسنده , , Masanori and Takeshima، نويسنده , , Hideo and Katagiri، نويسنده , , Hideki and Asano، نويسنده , , Tomoichiro and Oka، نويسنده , , Yoshitomo and Maruyama، نويسنده , , Ikuro and Kuratsu، نويسنده , , Jun-ichi، نويسنده ,
Abstract :
We report the increased activity and expression of the ILK protein in human glioblastomas and demonstrate that ILK activity is regulated by PTEN. The transfection of wild type-PTEN into the glioblastoma cell line U-251 MG altered the localization of ILK in the cell membrane; transfection with PTEN down-regulated PKB/Akt-Ser-473 phosphorylation via the inhibition of ILK-signaling. Our results suggest that ILK is critical for the PTEN-sensitive regulation of PKB/Akt-dependent cell survival. The selective COX-2 inhibitor NS-398 was found capable of down-regulating ILK and PKB/Akt phosphorylation. Our data indicate that inhibition of ILK signaling may be beneficial in the treatment of PTEN-deficient glioblastoma.
Keywords :
Glioblastoma , ILK , PTEN , NS-398 , PKB/Akt-Serine 473