PDK1-SGK1 Signaling Sustains AKT-Independent mTORC1 Activation and Confers Resistance to PI3Kα Inhibition
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- 作者：Pau Castel1 ; Haley Ellis1 ; Ruzica Bago2 ; Eneda Toska1 ; Pedram Razavi1 ; 3 ; F. Javier Carmona1 ; Srinivasaraghavan Kannan4 ; Chandra S. Verma4 ; 5 ; 6 ; Maura Dickler3 ; Sarat Chandarlapaty1 ; 3 ; Edi Brogi7 ; Dario R. Alessi2 ; José ; Baselga1 ; 3 ; baselgaj@mskcc.org" class="auth_mail" title="E-mail the corresponding author ; Maurizio Scaltriti1 ; 7 ; scaltrim@mskcc.org" class="auth_mail" title="E-mail the corresponding author
- 刊名：Cancer Cell
- 出版年：2016
- 出版时间：8 August 2016
- 年：2016
- 卷：30
- 期：2
- 页码：229-242
- 全文大小：3817 K
文摘
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The PDK1-SGK1 axis can sustain mTORC1 activity upon PI3K/AKT suppression
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SGK1 directly phosphorylates TSC2, resulting in mTORC1 activation
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Targeting PDK1 sensitizes PIK3CA-mutant cells to PI3Kα inhibition