Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10959227 | Seminars in Cell & Developmental Biology | 2012 | 10 Pages |
Abstract
⺠Oxidative stress can mediate the viability of ECM-detached cancer cells. ⺠Metabolic pathways are altered in ECM-detached cancer cells to promote survival and metastatic disease. ⺠Non-canonical cell death mechanisms including autophagy, entosis, and necroptosis have been shown or implicated to be involved in cell death caused by ECM-detachment. ⺠AMPK and HIF1 mediated signaling can modulate the survival of ECM-detached cancer cells.
Keywords
RHIMPDHTIGARSGLT1ANGPTL4mTORC1TP53-induced glycolysis and apoptosis regulatorECMATGHIF-1αBMFMLKLPDK4TCAPPPRho associated protein kinaseAMPKPI(3)Kunc-51-like kinase 1PYGLTNFαGLUD1glutamate dehydrogenase 1BDNFROSAnoikisangiopoietin-like 4tricarboxylic acidtumor necrosis factor alphaCancer metabolismendoplasmic reticulumhypoxia-inducible factor 1 alphabrain derived neurotrophic factorphosphatidylinositol 3 kinaseextra cellular matrixExtracellular matrixMetastasismixed lineage kinase domain-likeCell deathpentose phosphate pathwayMammalian target of rapamycin complex 1Pleckstrin HomologyAutophagy-related proteinsadenosine monophosphate-activated protein kinasepyruvate dehydrogenasePyruvate dehydrogenase kinase 4pyruvate kinaseGlulGlycogen phosphorylaseReactive oxygen speciesRock
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Authors
Cassandra L. Buchheit, Raju R. Rayavarapu, Zachary T. Schafer,