Highly read on genesdev.cshlp.org 27—31 May

Tumours subject to stressors such as starvation survive by altering their metabolic activities — and they do so by boosting the expression of an enzyme that normally functions in the brain.

Tak Mak at the University of Toronto in Ontario, Canada, and his colleagues found increased expression of CPT1C in human lung tumours, and that this elevated expression boosts fatty-acid metabolism and leads to drug resistance. Silencing CPT1C renders cancer cells vulnerable to drugs such as rapamycin, low nutrient levels and low oxygen levels.

When human breast cancer cells with silenced CPT1C were implanted into mice, they grew at a slower rate than those expressing CPT1C. The results suggest that CPT1C mediates tumour-cell survival and could be a useful therapeutic target.

Genes Dev. 25, 1041–1051 (2011)