Tumour cells generally use altered metabolic pathways for energy production, in particular they display a switch in the way glucose is metabolized. Although this aberration was first noticed by Otto Warburg some 80 years ago, two papers in Nature shed further light on the mechanisms underlying this switch.
Lewis Cantley and colleagues looked at pyruvate kinase - an enzyme involved in glucose metabolism - which exists in some cancer cells in an embryonic form known as M2. By making the cells produce the adult (M1) form instead, the team were able to set cancer cells back on to their normal metabolic course and curb the cells' tumour-forming capacity. In an accompanying paper, they reveal how M2 pyruvate kinase is subject to internal controls that do not affect M1, which may explain the different modes of glucose metabolism in cancer cells.
The discovery that M2 aids tumour growth demonstrates the importance of the specialized metabolism of cancer cells, say the authors.
Lewis Cantley (Beth Israel Deaconess Medical Center, Boston, MA, USA)
(C) Nature press release.
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