| Literature DB >> 24656822 |
Abbas Hadji1, Paolo Ceppi1, Andrea E Murmann1, Sonia Brockway1, Abhinandan Pattanayak1, Bhavneet Bhinder2, Annika Hau1, Shirley De Chant1, Vamsi Parimi3, Piotre Kolesza3, Joanne Richards4, Navdeep Chandel5, Hakim Djaballah2, Marcus E Peter6.
Abstract
CD95 (Fas/APO-1), when bound by its cognate ligand CD95L, induces cells to die by apoptosis. We now show that elimination of CD95 or CD95L results in a form of cell death that is independent of caspase-8, RIPK1/MLKL, and p53, is not inhibited by Bcl-xL expression, and preferentially affects cancer cells. All tumors that formed in mouse models of low-grade serous ovarian cancer or chemically induced liver cancer with tissue-specific deletion of CD95 still expressed CD95, suggesting that cancer cannot form in the absence of CD95. Death induced by CD95R/L elimination (DICE) is characterized by an increase in cell size, production of mitochondrial ROS, and DNA damage. It resembles a necrotic form of mitotic catastrophe. No single drug was found to completely block this form of cell death, and it could also not be blocked by the knockdown of a single gene, making it a promising way to kill cancer cells.Entities:
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Year: 2014 PMID： 24656822 PMCID： PMC4083055 DOI： 10.1016/j.celrep.2014.02.035
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423