Literature DB >> 26609545

Metabolic vulnerability of KRAS-driven cancer cells.

David A Foster1.   

Abstract

Interfering with anaplerotic utilization of glutamine (Gln) was recently reported to sensitize KRAS-driven cancer cells to the cytotoxic effects of capecitabine and paclitaxel. This effect was due to bypass of a Gln-dependent G1 cell cycle checkpoint in these cells. This study highlights therapeutic opportunities created by metabolic reprogramming in cancer cells.

Entities:  

Keywords:  Glutamine; KRAS; TCA cycle; anaplerosis; cell cycle

Year:  2014        PMID： 26609545      PMCID： PMC4655600          DOI： 10.4161/23723548.2014.963445

Source DB:  PubMed          Journal:  Mol Cell Oncol        ISSN： 2372-3556


  10 in total

Review 1.  Glutamine and cancer: cell biology, physiology, and clinical opportunities.

Authors:  Christopher T Hensley; Ajla T Wasti; Ralph J DeBerardinis
Journal:  J Clin Invest       Date:  2013-09-03       Impact factor: 14.808

2.  Regulation of G1 Cell Cycle Progression: Distinguishing the Restriction Point from a Nutrient-Sensing Cell Growth Checkpoint(s).

Authors:  David A Foster; Paige Yellen; Limei Xu; Mahesh Saqcena
Journal:  Genes Cancer       Date:  2010-11

Review 3.  Metabolic reprogramming: a cancer hallmark even warburg did not anticipate.

Authors:  Patrick S Ward; Craig B Thompson
Journal:  Cancer Cell       Date:  2012-03-20       Impact factor: 31.743

Review 4.  ras oncogenes in human cancer: a review.

Authors:  J L Bos
Journal:  Cancer Res       Date:  1989-09-01       Impact factor: 12.701

Review 5.  Dragging ras back in the ring.

Authors:  Andrew G Stephen; Dominic Esposito; Rachel K Bagni; Frank McCormick
Journal:  Cancer Cell       Date:  2014-03-17       Impact factor: 31.743

6.  Beyond aerobic glycolysis: transformed cells can engage in glutamine metabolism that exceeds the requirement for protein and nucleotide synthesis.

Authors:  Ralph J DeBerardinis; Anthony Mancuso; Evgueni Daikhin; Ilana Nissim; Marc Yudkoff; Suzanne Wehrli; Craig B Thompson
Journal:  Proc Natl Acad Sci U S A       Date:  2007-11-21       Impact factor: 11.205

Review 7.  Exploiting synthetic lethal interactions for targeted cancer therapy.

Authors:  H Christian Reinhardt; Hai Jiang; Michael T Hemann; Michael B Yaffe
Journal:  Cell Cycle       Date:  2009-10-01       Impact factor: 4.534

8.  Blocking anaplerotic entry of glutamine into the TCA cycle sensitizes K-Ras mutant cancer cells to cytotoxic drugs.

Authors:  M Saqcena; S Mukhopadhyay; C Hosny; A Alhamed; A Chatterjee; D A Foster
Journal:  Oncogene       Date:  2014-07-14       Impact factor: 9.867

9.  Glutamine supports pancreatic cancer growth through a KRAS-regulated metabolic pathway.

Authors:  Jaekyoung Son; Costas A Lyssiotis; Haoqiang Ying; Xiaoxu Wang; Sujun Hua; Matteo Ligorio; Rushika M Perera; Cristina R Ferrone; Edouard Mullarky; Ng Shyh-Chang; Ya'an Kang; Jason B Fleming; Nabeel Bardeesy; John M Asara; Marcia C Haigis; Ronald A DePinho; Lewis C Cantley; Alec C Kimmelman
Journal:  Nature       Date:  2013-03-27       Impact factor: 49.962

10.  Amino acids and mTOR mediate distinct metabolic checkpoints in mammalian G1 cell cycle.

Authors:  Mahesh Saqcena; Deepak Menon; Deven Patel; Suman Mukhopadhyay; Victor Chow; David A Foster
Journal:  PLoS One       Date:  2013-08-19       Impact factor: 3.240
  10 in total
  2 in total

1.  Inhibiting glutamine utilization creates a synthetic lethality for suppression of ATP citrate lyase in KRas-driven cancer cells.

Authors:  Ahmet Hatipoglu; Deepak Menon; Talia Levy; Maria A Frias; David A Foster
Journal:  PLoS One       Date:  2022-10-21       Impact factor: 3.752

Review 2.  Mechanisms of Resistance to KRASG12C Inhibitors.

Authors:  Victoria Dunnett-Kane; Pantelis Nicola; Fiona Blackhall; Colin Lindsay
Journal:  Cancers (Basel)       Date:  2021-01-05       Impact factor: 6.639
  2 in total

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