Metformin inhibits mammalian target of rapamycin-dependent translation initiation in breast cancer cells.

By R. Dowling, M. Zakikhani, I. Fantus, Michael Pollak, Nahum Sonenberg. Cancer Research, 2007

954 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/05de5cce02db99d42beb9aa3910a947e19cc086f

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Citations in the corpus

Metformin, Independent of AMPK, Inhibits mTORC1 In a Rag GTPase-Dependent Manner (2010, background): “Efforts to reconcile this observation with that of Dowling et al. (Dowling et al., 2007) led to our finding that, as the density of cells in culture increases, mTORC1 signaling in TSC2-deficient cells acquires sensitivity to metformin inhibition (Figures 3C and 3D).”
The insulin and insulin-like growth factor receptor family in neoplasia: an update (2012, background): “Although metformin also has inhibitory effects on respiratory complex I that are similar to those observed in hepatocytes in other untransformed and neoplastic cell type”
Targeting metabolic transformation for cancer therapy (2010, background): “A further study on diabetic patients with breast cancer as well as studies on breast cancer cells in vitro and a mouse model of breast cancer also found an anti-tumour effect of metformi”
G protein-coupled receptors: novel targets for drug discovery in cancer (2010, background): “It is noteworthy that metformin (1,1-dimethylbiguanide hydrochloride), one of the most widely prescribed drugs for the treatment of type 2 diabetes, activates AMP kinase (AMPK), which in turn blocks mTOR complex 1 activity, leading to the inhibition of cancer cell growt”
mTOR: a pharmacologic target for autophagy regulation. (2015, positive): “Thus, metformin treatment inhibits mTORC1-mediated protein synthesis in breast cancer cells (111).”
Cellular and molecular mechanisms of metformin: an overview. (2012, background): “The antineoplastic activity of metformin via AMPK activation is mediated through the inhibition of mTORC1 signaling, leading to inhibition of protein synthesis and cell proliferation [121, 123, 124].”
Diabetes and Cancer (2010, neutral): “These studies suggest that metformin-induced activation of AMPactivated protein kinase (AMPK) in tumor cells may lead to growth inhibition, at least in part by inhibiting protein synthesis (84).”
Insulin and insulin-like growth factor signalling in neoplasia (2008, background): “and attenuates the reponse of cancer cells to insulin in vitro”