1. Cancer Cells Hijack Gluconeogenic Enzymes to Fuel Cell Growth
Eduardo Balsa-Martinez, Pere Puigserver 
Molecular Cell 
Volume 60, Issue 4, Pages (November 2015)
DOI: /j.molcel
Copyright © 2015 Elsevier Inc. Terms and Conditions

2. Figure 1
PEPCK and PCK2 Enable PEP Conversion from Non-carbohydrate Substrates to Support Tumor Growth
Cytoplasmic PEPCK enhances TCA cycle flux and anabolic metabolism in colon cancer cells. PEPCK-dependent increases in cellular glutamine levels activate mTOR1 and promote cell proliferation. Alternatively, PCK2 is upregulated by HIF-1α and HIF-2α in lung cancer cells upon glucose withdrawal. Under these conditions, glutamine serves as an anaplerotic substrate to replenish TCA cycle intermediates. PCK2-derived PEP increases glucose intermediates to support anabolic metabolism and cell proliferation.
Molecular Cell  , DOI: ( /j.molcel )
Copyright © 2015 Elsevier Inc. Terms and Conditions