Tumor cell metabolism: cancer's Achilles' heel.
The essential hallmarks of cancer are intertwined with an altered cancer cell-intrinsic metabolism, either as a consequence or as a cause. As an example, the resistance of cancer mitochondria against apoptosis-associated permeabilization and the altered contribution of these organelles to metabolism are closely related. Similarly, the constitutive activation of signaling cascades that stimulate cell growth has a profound impact on anabolic metabolism. Here, we review the peculiarities of tumor cell metabolism that might be taken advantage of for cancer treatment. Specifically, we discuss the alterations in signal transduction pathways and/or enzymatic machineries that account for metabolic reprogramming of transformed cells.
INSERM, U848, F-94805 Villejuif, France. kroemer@igr.fr
Guido
G
Kroemer
Jacques
J
Pouyssegur
D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D017209:Apoptosis / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D015195:Drug Design; D004734:Energy Metabolism / Q000187:drug effects*; D004791:Enzyme Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D006801:Humans; D008928:Mitochondria / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D009361:Neoplasm Invasiveness; D009362:Neoplasm Metastasis; D009369:Neoplasms / Q000098:blood supply / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D009389:Neovascularization, Pathologic / Q000378:metabolism / Q000517:prevention & control; D015398:Signal Transduction / Q000187:drug effects; D019139:Tumor Escape / Q000187:drug effects
D000970:Antineoplastic Agents; D004791:Enzyme Inhibitors