Akt Stimulates Aerobic Glycolysis in Cancer Cells

By R. Elstrom, Daniel E. Bauer, M. Buzzai, Robyn Karnauskas, Marian H. Harris, D. Plas, H. Zhuang, Ryan M. Cinalli, A. Alavi, C. Rudin and 1 more. Cancer Research, 2004

1,494 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/2bbf353c251a2631c5315e412ef3f7fa75e0c8f5

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Citations in the corpus

Autophagy promotes tumor cell survival and restricts necrosis, inflammation, and tumorigenesis. (2006, background): “Indeed, the metabolic state of tumor cells, specifically stimulation of aerobic glycolysis by AKT (Elstrom et al., 2004), promotes necrotic cell death in response to DNA alkylating agents that may be the basis for their successful use in chemotherapy regimens (Zong et al., 2004).”
Tumour hypoxia induces a metabolic shift causing acidosis: a common feature in cancer (2009, background): “Thus, Akt activation is sufficient to explain in part the ‘Warburg effect’ [69, 74, 75] that leads to acidosis of the tumour environment.”
The biology of cancer: metabolic reprogramming fuels cell growth and proliferation. (2008, background): “Second, through effects on gene expression and enzyme activity, Akt increases glycolysis and lactate production and is sufﬁcient to induce a Warburg effect in either nontransformed cells or cancer cells (Elstrom et al., 2004; Plas et al., 2001; Rathmell et al., 2003).”
Otto Warburg's contributions to current concepts of cancer metabolism (2011, background): “Recent in vitro data on glucose uptake and lactic acid release by human glioblastoma LN18 cells show a similar 13% increase in ATP productio”
Multiparameter metabolic analysis reveals a close link between attenuated mitochondrial bioenergetic function and enhanced glycolysis dependency in human tumor cells. (2007, background): “Multiple oncogenic pathways including Ras, Src, and Myc have been shown to promote malignant transformation and aerobic glycolysis through stabilization of hypoxia-inducible factor 1 (HIF-1 ) (3, 10, 11).”
ATP citrate lyase inhibition can suppress tumor cell growth. (2005, background): “Upregulation of glycolytic metabolism occurs downstream of multiple oncogenic pathways (Dang and Semenza, 1999; Elstrom et al., 2004) and has been shown to correlate with increased tumor aggressiveness and poor patient prognosis in several tumor types (Detterbeck et al.”
HIF-1-mediated expression of pyruvate dehydrogenase kinase: a metabolic switch required for cellular adaptation to hypoxia. (2006, background): “physiologic adaptation of normal cells to hypoxia and may also provide new insights into the Warburg effect or the reliance of cancer cells on glycolytic metabolism even under aerobic conditions (Dang and Semenza, 1999; Elstrom et al., 2004).”
Autophagy in metazoans: cell survival in the land of plenty (2005, background): “A similar phenomenon is observed in glioblastoma cells that have constitutive Akt activity; the absence of glucose causes rapid cell death regardless of an abundance of alternate fuels such as fatty acids and amino acid”
HIF-1 inhibits mitochondrial biogenesis and cellular respiration in VHL-deficient renal cell carcinoma by repression of C-MYC activity. (2007, background): “Glucose transport and aerobic glycolysis are also stimulated by oncogenic alterations that increase AKT kinase activity (Elstrom et al., 2004).”
Fuel feeds function: energy metabolism and the T-cell response (2005, background): “This phenomenon, which is known as AEROBIC GLYCOLYSIS , is also characteristic of many transformed cell”
The extracellular matrix modulates the hallmarks of cancer (2014, positive): “Intriguingly, tumor cells interacting with a stiffened ECM show a marked upregulation of growth factor-dependent PI3K/Akt signaling, which by virtue of its ability to increase aerobic glycolysis suggests that tissue tension may also directly regulate tumor cell metabolism [108].”
Fatty acid synthase and the lipogenic phenotype in cancer pathogenesis (2007, background): “For example, the Akt oncogene directly renders cancer cells dependent on aerobic glycolysis, upregulates lipogenic gene expression in a SREBP1c-dependent manner, and directly activates ACLY, thus linking the upregulation of lipogenesis to the increase in glycolysi”
Causes and Consequences of Increased Glucose Metabolism of Cancers (2008, background): “Phosphorylated Akt stimulates glucose consumption in transformed cells without affecting the rate of oxidative phosphorylation (138).”
Analysis of cancer metabolism by imaging hyperpolarized nuclei: prospects for translation to clinical research. (2011, background): “For example, glucose uptake is stimulated by the activation of oncogenic signaling [17,66] or by hypoxia, which suppresses the entry of glucose carbon into oxidative pathways and inhibits proliferation [67].”
Malignant astrocytic glioma: genetics, biology, and paths to treatment. (2007, background): “In addition to these maladapted biophysical properties of GBM microvasculature, specific genetic mutations in GBM likely contribute to compromised tumor bioener-getics, specifically the shift in energy reduction from oxidative phosphorylation to glycolysis (Elstrom et al. 2004; Fantin et al. 2006).”