| Literature DB >> 27652328 |
Alenka Lovy1, J Kevin Foskett2, César Cárdenas3.
Abstract
Mitochondrial metabolism is essential to fulfill the large demand for macromolecule biosynthesis in cancer. We recently identified low-level InsP3R-mediated Ca(2+) transfer to mitochondria as an unexpected requirement for mitochondrial function. Here we reveal that its absence specifically targets cancer cells and causes necrosis at daughter cell separation during ongoing proliferation.Entities:
Keywords: AMPK; MCU; OXPHOS; autophagy; cell cycle; necrosis
Year: 2016 PMID: 27652328 PMCID: PMC4972124 DOI: 10.1080/23723556.2016.1185563
Source DB: PubMed Journal: Mol Cell Oncol ISSN: 2372-3556