Exploiting mitochondrial apoptosis for the treatment of cancer.
Mitochondria are key regulators of many forms of cell death and often altered in human malignancies. Since the inefficacy of established cancer therapies is, at least to a large extent, the result of oncogenic blockade of cell death pathways, compounds that directly affect mitochondrial functions are considered to present a promising alternative approach to eradicate chemotherapy-resistant cancer cells. Since mitochondria-targeted drugs can directly initiate mitochondrial perturbations independent of upstream signaling events, these agents may induce cell death and overcome drug resistance under circumstances, where conventional drugs fail to act because pathways upstream of mitochondria are frequently disrupted in cancer cells. A better understanding of the fundamental mechanisms that govern the complex processes of mitochondrial apoptosis is expected to open new perspectives for cancer drug development. Hopefully, this knowledge will eventually be translated into medical application for the treatment of human cancer.
Fulda
Simone
S
Institute for Experimental Cancer Research in Pediatrics, Goethe-University Frankfurt, Germany. s.fulda@kinderkrebsstiftung-frankfurt.de
D000970:Antineoplastic Agents / Q000737:chemistry / Q000378:metabolism* / Q000493:pharmacokinetics*; D017209:Apoptosis / Q000187:drug effects*; D006801:Humans; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism*; D009369:Neoplasms / Q000188:drug therapy*
D000970:Antineoplastic Agents