Author/Authors :
Jin، نويسنده , , Hyeon-Ok and Hong، نويسنده , , Sung-Eun and Kim، نويسنده , , Jae-Hee and Choi، نويسنده , , Ha-Na and Kim، نويسنده , , Karam and An، نويسنده , , Sungkwan and Choe، نويسنده , , Tae-Boo and Hwang، نويسنده , , Chang-Sun and Lee، نويسنده , , Jae Ho and Kim، نويسنده , , Jong-il and Kim، نويسنده , , Hyun Ah and Kim، نويسنده , , Eun-Kyu and Noh، نويسنده , , Woo Chul and Hong، نويسنده , , Young-Joon and Hong، نويسنده , , Seok-Il and Lee، نويسنده , , Jin Kyung and Park، نويسنده , , In-Chul، نويسنده ,
Abstract :
Herein, we show that the constitutive overexpression of Redd1, a negative regulator of mTORC1, induces Akt activation in lung cancer cells. Akt phosphorylation was reduced to basal levels by Rictor siRNA, suggesting the involvement of mTORC2 in this process. Perifosine and PP242, selective inhibitors of Akt and mTORC1/2, respectively, efficiently suppressed the Akt phosphorylation that was induced by the sustained overexpression of Redd1 and increased the sensitivity of the cells to cisplatin. Therefore, the sustained overexpression of Redd1 leads to mTORC1 inhibition and to consequent Akt activation that is involved in cell survival. This finding highlights the importance of Akt activation as a therapeutic target to overcome resistance to chemotherapy.
