Cancer cells are highly proliferative,invasive,metastatic and initiate angiogenesis.These activities demand plentiful energy and bountiful stores of anabolic precursors,a situation that puts significant strain on meta...Cancer cells are highly proliferative,invasive,metastatic and initiate angiogenesis.These activities demand plentiful energy and bountiful stores of anabolic precursors,a situation that puts significant strain on metabolic pathways and necessitates juggling of finite resources.However,the location and erratic structural organisation of tumours means they reside in a nutrient-poor environment.The glycolytic phenotype has evolved in cancer cells to provide a suitable balance between bioenergetic and biosynthetic pathways.Does this adopted strategy also support the overexpression of an ATP-dependent transporter(P-glycoprotein)to maintain resistance against chemotherapy?This article highlights the metabolic adaptations used by cancer cells to maintain both a glycolytic phenotype and sustain the activity of P-glycoprotein.We argue that these cells negotiate an energy precipice to achieve these adaptations.Finally,we advocate the use of compounds that place resistant cells expressing P-glycoprotein under further metabolic strain and how uncoupling protein-2 may provide an ideal target for them.展开更多
文摘Cancer cells are highly proliferative,invasive,metastatic and initiate angiogenesis.These activities demand plentiful energy and bountiful stores of anabolic precursors,a situation that puts significant strain on metabolic pathways and necessitates juggling of finite resources.However,the location and erratic structural organisation of tumours means they reside in a nutrient-poor environment.The glycolytic phenotype has evolved in cancer cells to provide a suitable balance between bioenergetic and biosynthetic pathways.Does this adopted strategy also support the overexpression of an ATP-dependent transporter(P-glycoprotein)to maintain resistance against chemotherapy?This article highlights the metabolic adaptations used by cancer cells to maintain both a glycolytic phenotype and sustain the activity of P-glycoprotein.We argue that these cells negotiate an energy precipice to achieve these adaptations.Finally,we advocate the use of compounds that place resistant cells expressing P-glycoprotein under further metabolic strain and how uncoupling protein-2 may provide an ideal target for them.
