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Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Cell+Rep 2017 ; 18 (2): 468-81 Nephropedia Template TP
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The Anti-Warburg Effect Elicited by the cAMP-PGC1? Pathway Drives Differentiation of Glioblastoma Cells into Astrocytes #MMPMID28076790
Xing F; Luan Y; Cai J; Wu S; Mai J; Gu J; Zhang H; Li K; Lin Y; Xiao X; Liang J; Li Y; Chen W; Tan Y; Sheng L; Lu B; Lu W; Gao M; Qiu P; Su X; Yin W; Hu J; Chen Z; Sai K; Wang J; Chen F; Chen Y; Zhu S; Liu D; Cheng S; Xie Z; Zhu W; Yan G
Cell Rep 2017[Jan]; 18 (2): 468-81 PMID28076790show ga
Glioblastoma multiforme (GBM) is among the most aggressive of human cancers. Although differentiation therapy has been proposed as a potential approach to treat GBM, the mechanisms of induced differentiation remain poorly defined. Here, we established an induced differentiation model of GBM using cAMP activators that specifically directed GBM differentiation into astroglia. Transcriptomic and proteomic analyses revealed that oxidative phosphorylation and mitochondrial biogenesis are involved in induced differentiation of GBM. Dibutyryl cyclic AMP (dbcAMP) reverses the Warburg effect, as evidenced by increased oxygen consumption and reduced lactate production. Mitochondrial biogenesis induced by activation of the CREB-PGC1? pathway triggers metabolic shift and differentiation. Blocking mitochondrial biogenesis using mdivi1 or by silencing PGC1? abrogates differentiation; conversely, overexpression of PGC1? elicits differentiation. In GBM xenograft models and patient-derived GBM samples, cAMP activators also induce tumor growth inhibition and differentiation. Our data show that mitochondrial biogenesis and metabolic switch to oxidative phosphorylation drive the differentiation of tumor cells.