Multiparameter metabolic analysis reveals a close link between attenuated mitochondrial bioenergetic function and enhanced glycolysis dependency in human tumor cells.

By Min Wu, Andy Neilson, Amy L. Swift, R. Moran, James Tamagnine, D. Parslow, S. Armistead, Kristie Lemire, Jim Orrell, J. Teich and 2 more. American Journal of Physiology - Cell Physiology, 2007

935 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/532f00329023dd4c7f6a426f97e11c9964031677

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Citations in the corpus

Causes and Consequences of Increased Glucose Metabolism of Cancers (2008, background): “For example, upregulation of glycolysis in response to mitochondrial inhibition is dependent on AMPK activity (96).”
Activated Ras requires autophagy to maintain oxidative metabolism and tumorigenesis. (2011, methodology): “Tumors have different levels of mitochondrial bioenergetic function (Wu et al. 2007), attributable to oncogenic mutations and activation of signaling pathways that control metabolism (Vander Heiden et al. 2009) or mutations in TCA cycle enzymes (Gottlieb and Tomlinson 2005) that promote aerobic…”
The energy sensor AMPK regulates T cell metabolic adaptation and effector responses in vivo. (2015, methodology): “To explore this further, we cultured Teff cells for 5 hr under various glucose concentrations, and assessed their bioenergetic profiles via Seahorse assay (Wu et al., 2007).”
The Glucose Transporter Glut1 is Selectively Essential for CD4 T Cell Activation and Effector Function (2014, methodology): “Extracellular Flux Analysis Oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) were measured with an XF24 extracellular flux analyzer (Seahorse Bioscience) using CellTak (BDBiosciences) in unbuffered RPMI (Sigma-Aldrich) supplemented with 10mM Dglucose (Sigma-Aldrich) and 10mM”
Mitochondria in cancer cells: what is so special about them? (2008, positive): “However, when glycolysis was suppressed, tumor cells were unable to sufficiently upregulate mitochondrial oxidative phosphorylation, indicating partial mitochondrial impairment [ 16 ].”
Tumor-derived hydrogen sulfide, produced by cystathionine-β-synthase, stimulates bioenergetics, cell proliferation, and angiogenesis in colon cancer (2013, methodology): “Cellular migration and invasion assays were performed as described (47).”
Cardiac natriuretic peptides act via p38 MAPK to induce the brown fat thermogenic program in mouse and human adipocytes. (2012, neutral): “Cellular OCRs and ECARs were measured as described previously (44, 75).”
Cancer as a metabolic disease (2010, background): “Considerable controversy has surrounded the issue of mitochondrial function in cancer cells [18,29,30,33,34,51-57].”
AMPK is a negative regulator of the Warburg Effect and suppresses tumor growth in vivo (2012, background): “Lymphomas expressing AMPKa1 shRNA displayed an elevated extracellular acidification rate (ECAR, Figure 2B), an index of lactate production (Wu et al., 2007), but displayed no significant difference in their oxygen consumption rate (OCR; Figures 2C and S2A).”
Use of Cells Expressing γ Subunit Variants to Identify Diverse Mechanisms of AMPK Activation (2010, methodology): “Oxygen consumption rates were continuously measured as described previously (Wu et al., 2007).”