Apoptin ond Its Mechanism of Action

Classical chemotherapy, that spocifically targets rapidly proliferating cells, has been in existence for over eighty yeors and has proven to be fully successful in only a limited number of cancers. Thus, this review focuses on a novel, emerging approach for cancer therapy that uses alternative, a nd more unique features of cancer cells. This new approach faci litates the seloctive targeting of cancer, while sparing normal, non-transformed cells. Examples of molocules that kill cancer cells seloctively are: apoptin, E40rf4, viral protein R {VpR), and Brevinin-2R. Be low we focus on apoptin, a product of the third open reading frame (VP3) of the chicken anemia virus. Besides discussing apoptin's mechanism of action, we also provide concise insight into the biology of a chicken anemia virus infoction. Since apoptin's cancer-seloctive toxicity depends on its nuclear localization, we broadly discuss mochanism!s) involved in its nuclear retention (both nuclear import and export). We also discuss recent findings on apoptin's molecular mochanism of action, with a focus on the role of Nur77 in apoptin's nucleo<ytapiasmic signaling. Finally, we compare the current findings on opoptin to the mechanism of cancer seloctive toxicity of E40rf4. In the 'summory' -soction, besides highlighting important issues related to cancerseloctive therapy, we also discuss concurrent approaches towards therapy personalization, particularly those related to the in vivo-, and realtime cancer.theropy efficacy monitoring, using "Iab..on-the<hipu and other emerging tochnologies.