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- W2105530711 abstract "Abstract Biguanides, including metformin, buformin, and phenformin, are potential antitumorigenic agents and induce cell death during glucose deprivation, a cell condition that occurs in the tumor microenvironment. Here, we show that this selective killing of glucose-deprived cells is coupled with hyperactivation of eukaryotic initiation factor 4E-binding protein 1 (4E-BP1), a negative regulator of translation initiation. We found, in fact, that the 4E-BP1 hyperactivation led to failure of the unfolded protein response (UPR), an endoplasmic reticulum–originated stress signaling pathway for cell survival. We also found that the 4E-BP1–mediated UPR inhibition occurred through a strong inhibition of the mTOR signaling pathway, a proven antitumor target. Importantly, the 4E-BP1 hyperactivation can be also seen in xenografted cancer cells through an in vivo biguanide treatment. Our findings indicate that antitumor action of biguanides can be mediated by 4E-BP1 hyperactivation, which results in UPR inhibition and selective cell killing when glucose is withdrawn. Mol Cancer Ther; 11(5); 1082–91. ©2012 AACR." @default.
- W2105530711 created "2016-06-24" @default.
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- W2105530711 date "2012-05-01" @default.
- W2105530711 modified "2023-10-02" @default.
- W2105530711 title "Hyperactivation of 4E-Binding Protein 1 as a Mediator of Biguanide-Induced Cytotoxicity during Glucose Deprivation" @default.
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- W2105530711 doi "https://doi.org/10.1158/1535-7163.mct-11-0871" @default.
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