A key role for mitochondrial gatekeeper pyruvate dehydrogenase in oncogene-induced senescence

By Joanna Kaplon, Liang Zheng, Katrin Meissl, B. Chaneton, V. Selivanov, G. Mackay, S. H. Burg, E. Verdegaal, Marta Cascante, Tomer Shlomi and 2 more. Nature, 2013

600 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/500b72e948c0620c27b4475b593751217858965c

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In Cancer Research

1. L. Galluzzi
2. Guido Kroemer
3. Huafeng Zhang
4. Ping Gao
5. Jason W. Locasale
6. J. B. Pedro
7. Maria Liberti
8. P. Porporato

In Molecular Biology

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2. Guido Kroemer
3. Huafeng Zhang
4. Ping Gao
5. Linchong Sun
6. J. B. Pedro
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8. N. Filigheddu

In Physiology

1. L. Galluzzi
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4. Rafik Amir Salama
5. A. Alimonti
6. J. Kohli
7. E. Zagato
8. Huafeng Zhang

Citations in the corpus

• Senescence and apoptosis: dueling or complementary cell fates? (2014, unknown): “For example, is pyruvate dehydrogenase suppressed in replicative senescence or PTEN-loss-induced senescence [18]? Regardless of differences in signaling pathways, Ras overexpression, BRAF mutation, and Pten deletion ultimately activate common effectors of senescence such as p19 and p16 [22].”
• The Warburg Effect: How Does it Benefit Cancer Cells? (2016, background): “OIS has a tumor-suppressive cellular function and a recent study has reported that increased glucose oxidation through pyruvate dehydrogenase (PDH) can regulate OIS.”
• Mitochondrial metabolism and cancer (2017, background): “(PDK1) or inhibit pyruvate dehydrogenase phosphatase catalytic subunit 2 (PDP2), resulting in limited pyruvate utilization by mitochondria and reduced ROS production [59].”
• Metabolic reprogramming and epigenetic modifications on the path to cancer (2021, background): “The role of PDC in cancer progression remains inconclusive (Kim et al., 2006; Papandreou et al., 2006; Hitosugi et al., 2011; Kaplon et al., 2013; Sutendra et al., 2014).”
• Hallmarks of Cellular Senescence. (2018, unknown): “Indeed, high TCA cycle activity is essential for the tumor-suppressing action of senescent cells [93].”
• Cellular Senescence: Defining a Path Forward. (2019, unknown): “Mitochondria in senescentcellsarelessfunctional,showingdecreasedmembrane potential, increased proton leak, reduced fusion and fission rates, increased mass, and abundance of tricarboxylic acid (TCA) cycle metabolites (Kaplon et al., 2013; Passos et al., 2010).”
• Cellular Senescence: Aging, Cancer, and Injury. (2019, background): “Growing literature on the metabolism of cellular senescence reports that both glucose consumption and lactate production are elevated during senescence (57, 101, 179).”
• Cellular senescence and its effector programs (2014, background): “Although, the Peeper and Gottlieb groups (Kaplon et al. 2013) did not report the actual levels of ATP production in OIS cells, another recent study by Dörr et al. (2013) has shown an increase of ATP production in both TIS lymphomas and OIS HDFs.”
• Mechanisms and functions of cellular senescence. (2018, unknown): “In work related to this concept, Kaplon and colleagues (118) argued that senescent cells must reprogram metabolism in order to support their metabolic demands.”