Journal
CANCER CELL
Volume 19, Issue 3, Pages 401-415Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2011.01.018
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Funding
- Ministry of Education, Singapore [ARC18/08]
- Nanyang Technological University [RG127/05, RG82/07]
- Biomedical Research Council [10/1/22/19/644]
- German Research Aid (Deutsche Krebshilfe: Tumorstammzellverbund)
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Cancer is a leading cause of death worldwide. Tumor cells exploit various signaling pathways to promote their growth and metastasis. To our knowledge, the role of angiopoietin-like 4 protein (ANGPTL4) in cancer remains undefined. Here, we found that elevated ANGPTL4 expression is widespread in tumors, and its suppression impairs tumor growth associated with enhanced apoptosis. Tumor-derived ANGPTL4 interacts with integrins to stimulate NADPH oxidase-dependent production of O-2(-). A high ratio of O-2(-):H2O2 oxidizes/activates Src, triggering the PI3K/PKB alpha and ERK prosurvival pathways to confer anoikis resistance, thus promoting tumor growth. ANGPTL4 deficiency results in diminished O-2(-) production and a reduced O-2(-):H2O2 ratio, creating a cellular environment conducive to apoptosis. ANGPTL4 is an important redox player in cancer and a potential therapeutic target.
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