Journal
CELL REPORTS
Volume 16, Issue 9, Pages 2415-2427Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2016.07.082
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Funding
- Italian Association for Cancer Research (AIRC) [MFAG-13521]
- Italian Ministry of Health
- University of Ferrara
- Telethon [GGP15219/B]
- AIRC [IG-14442]
- Italian Cystic Fibrosis Research Foundation [19/2014]
- Italian Ministry of Education, University and Research [20129JLHSY_002, RBAP11FXBC_002, RBFR10EGVP_001]
- FISM-Fondazione Italiana Sclerosi Multipla-cod [2014/B/3]
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The precise molecular mechanisms that coordinate apoptosis and autophagy in cancer remain to be determined. Here, we provide evidence that the tumor suppressor promyelocytic leukemia protein (PML) controls autophagosome formation at mitochondria-associated membranes (MAMs) and, thus, autophagy induction. Our in vitro and in vivo results demonstrate how PML functions as a repressor of autophagy. PML loss promotes tumor development, providing a growth advantage to tumor cells that use autophagy as a cell survival strategy during stress conditions. These findings demonstrate that autophagy inhibition could be paired with a chemotherapeutic agent to develop anticancer strategies for tumors that present PML downregulation.
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