The LKB1 tumor suppressor negatively regulates mTOR signaling.

By R. Shaw, N. Bardeesy, B. Manning, L. Lopez, Monica Kosmatka, R. DePinho, Lewis C. Cantley. Cancer Cell, 2004

1,144 citations recorded by the source corpus.

Subfields: Molecular Biology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/b260087c48d85b7488519b1f54fb10cdeae2a0e4

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Citations in the corpus

Targeting PI3K/Akt/mTOR Signaling in Cancer (2014, background): “Another negative regulator, LKB1, is in an energy-sensing pathway upstream of TSC (14).”
Ras, PI(3)K and mTOR signalling controls tumour cell growth (2006, background): “However, in cells that lack LKB1, mTORC1 remains active because the AMPK checkpoint is defectiv”
Perturbations of the AKT signaling pathway in human cancer (2005, background): “AMPK activation reduces anabolic pathways, such as lipogenesis, cholesterol biosynthesis and protein synthesis, the latter effect mediated in part by phosphorylation of tuberin that enhances its inhibitory effect on mTOR (Inoki et al., 2003; Shaw et al., 2004).”
Metformin and pathologic complete responses to neoadjuvant chemotherapy in diabetic patients with breast cancer. (2009, background): “Under low-energy and other stress conditions, AMPK phosphorylates a number of targets to inhibit cellular growth and proliferation, including components of the growth-promoting mammalian target of rapamycin pathway.(38-40) Whether the apparent antitumor effect of metformin in our diabetic patients m”
Metformin is an AMP kinase-dependent growth inhibitor for breast cancer cells. (2006, background): “At the cellular level, physiologic or pharmacological activation of AMP kinase would serve to further attenuate signaling in networks downstream of insulin and/or IGF-I receptors, particularly at the level of mTOR (15).”
Autophagy in malignant transformation and cancer progression (2015, positive): “…inactivation of NF1 (an upstream inhibitor of RAS), STK11 (an activator of AMPK best known as LKB1), TSC1 or TSC2 promotes MTORCI signaling, hence stimulating cell proliferation and inhibiting autophagic responses (Xu et al , 1990; Inoki et al , 2002; Shaw et al , 2004; Johannessen et al , 2005).”
Regulation of the mTOR complex 1 pathway by nutrients, growth factors, and stress (2010, background): “AMPK directly phos-phorylates TSC2, which through an unknown mechanism leads to its activation and thus to the suppression of mTORC1 (Corradetti et al., 2004; Inoki et al., 2003b; Shaw et al., 2004) and is vital for cell survival under glucose deprivation conditions (Inoki et al., 2003b).”