Caspases and cancer: Mechanisms of inactivation and new treatment modalities
2004 (English)In: Experimental Oncology, ISSN 0204-3564, Vol. 26, no 2, 82-97 p.Article in journal (Refereed) Published
Elimination of superfluous or mutated somatic cells is provided by various mechanisms including apoptosis. Deregulation of apoptotic signaling pathways may contribute to oncogenesis. Aspartate specific cysteine proteases, termed caspases are the key effector molecules in apoptosis. The aim of this review is to summarize the various defects in caspase-dependent cell death machinery identified in the neoplastic cells. These include not only mutations, but also alterations of gene methylation, and altered mRNA stability. Among the molecules that we discuss are elements of the extrinsic death pathway like CD95 (APO-1/Fas), FADD, FLIPs, FLICE, other apical caspases, components of the intrinsic apoptotic pathway like Apaf-1, caspase-9, and modulators of apoptotic pathways like IAPs, Smac/DIABLO, OMI/HtrA2, and other apoptosis regulating proteins. We also discuss recent data on cancer-specific agents that target effector mechanisms of apoptosis. Particular emphasis is given to the prospects for combining cell suicide-activating approaches with classical cancer therapies.
Place, publisher, year, edition, pages
2004. Vol. 26, no 2, 82-97 p.
aberrant methylation, adenovirus-mediated transfer, anticancer drugs, Apoptosis, cancer patient, carcinoma-cells, caspase, caspase activators, cell lung-cancer, cell-permeable peptides, cytochrome-c, down-regulation, fusion proteins, gene therapy, in-vivo, malignant glioma-cells, mutation, preclinical study, radiation-induced apoptosis, signaling complex disc, siRNA, tumor cell
Cancer and Oncology Cell Biology Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy)
IdentifiersURN: urn:nbn:se:liu:diva-87003ISI: 000222911000001PubMedID: 15273659OAI: oai:DiVA.org:liu-87003DiVA: diva2:584208