Abstract #LB-186: c-Myc suppression of miR-23 enhances mitochondrial glutaminase and glutamine metabolism

By Ping Gao, Irina Tchernyshyov, T. Chang, Yun‐Sil Lee, Kayoko Kita, T. Ochi, K. Zeller, A. D. Marzo, J. V. Eyk, Joshua T. Mendell and 1 more. 2009

923 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/dfc9e3f0b633e1198b4bd31ea16c9a71d27a220d

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

Citations in the corpus

Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate (2012, background): “While the role of glutamine as a nitrogen donor is important for the proliferation of these cells, their viability depends on glutamine as a carbon source for mitochondrial metabolism (DeBerardinis et al., 2007; Fan et al., 2010; Gao et al., 2009; Wise et al., 2008; Yuneva et al., 2007).”
Q's next: The diverse functions of glutamine in metabolism, cell biology and cancer (2009, background): “On the other hand, in P-493 B-lymphoma cells and PC3 prostate cancer cells the loss of cell proliferation and viability triggered by glutamine deprivation or GLS knockdown could be partially reversed with antioxidants (Gao et al., 2009).”
Metabolic reprogramming and epigenetic modifications on the path to cancer (2021, background): “For example, in addition to regulating glucose, glutamine and serine metabolism at the transcriptional level (Gao et al., 2009; Stine et al., 2015; Sun et al., 2015; Wu et al., 2017), cMyc increases SDHA (succinate dehydrogenase complex, subunit A) acetylation by promoting SKP2 (S-phase kinaseassoci”
miR-24 inhibits cell proliferation by suppressing expression of E2F2, MYC and other cell cycle regulatory genes by binding to “seedless” 3′UTR microRNA recognition elements (2009, background): “MYC may also suppress miR-24 transcription (Gao et al., 2009).”
Reprogramming of fatty acid metabolism in cancer (2019, background): “Moreover, amplification of the MYC oncogene drives increased glutamine metabolism and anaplerosis by transcriptionally activating mitochondrial glutaminase (GLS1) and the SLC1A5 glutamine transporter.(60,61) Hyperactivation of the phosphoinositide 3-kinase and AKT (PI3K–AKT) pathway has also been im”
Mitochondria and Cancer (2016, background): “The proto-oncoprotein c-Myc induces the expression of glutamine transporters SLC1A5 and SLC7A5/SLC3A2 (Nicklin et al., 2009) and GLS (Gao et al., 2009).”
Metabolic reprogramming and cancer progression (2020, background): “Oncogene-driven expression of nutrient transporters (24, 50), the ability to derive energy from diverse nutrient sources—including scavenged protein, recycled organelles, and necrotic debris (51–54)—and metabolic cooperativity among cancer cells or between cancer cells and stromal cells (55, 56) lik”
Links between metabolism and cancer. (2012, background): “Myc was subsequently shown to activate genes involved in mitochondrial biogenesis and function as well as those involved in glutamine metabolism (Li et al. 2005; Wise et al. 2008; Gao et al. 2009).”
Glutaminolysis: A Hallmark of Cancer Metabolism. (2017, background): “Furthermore, overexpression of c-MYC promotes the expression of mitochondrial GLS through transcriptional repression of miR-23a and miR-23b (39).”