Abstract
The uncontrolled proliferation of cancer cells requires functional mitochondrial metabolism, which uses Ca(2+) as a cofactor. IP3 receptors (IP3Rs) from endoplasmic reticulum (ER) Ca(2+) stores provide the supply of Ca(2+) to mitochondria. A new study by Cardenas et al. shows that, in contrast to normal cells, cancer cells critically depend on ER-mitochondrial Ca(2+) fluxes for their survival by sustaining the production of mitochondrial substrates used for nucleotide biosynthesis and proliferation.
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