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dc.contributor.author Fiandalo, M.V.
dc.contributor.author Kyprianou, N.
dc.date.accessioned 2018-06-19T18:54:53Z
dc.date.available 2018-06-19T18:54:53Z
dc.date.issued 2012
dc.identifier.citation Caspase Control: Protagonists of Cancer Cell Apoptosis / M.V. Fiandalo, N. Kyprianou // Experimental Oncology. — 2012. — Т. 34, № 3. — С. 165-175. — Бібліогр.: 150 назв. — англ. uk_UA
dc.identifier.issn 1812-9269
dc.identifier.uri http://dspace.nbuv.gov.ua/handle/123456789/139061
dc.description.abstract Emergence of castration-resistant metastatic prostate cancer is due to activation of survival pathways, including apoptosis suppression and anoikis resistance, and increased neovascularization. Thus targeting of apoptotic players is of critical significance in prostate cancer therapy since loss of apoptosis and resistance to anoikis are critical in aberrant malignant growth, metastasis and conferring therapeutic failure. The majority of therapeutic agents act through intrinsic mitochondrial, extrinsic death receptor pathways or endoplasmic reticulum stress pathways to induce apoptosis. Current therapeutic strategies target restoring regulatory molecules that govern the pro-survival pathways such as PTEN which regulates AKT activity. Other strategies focus on reactivating the apoptotic pathways either by down-regulating anti-apoptotic players such as BCL-2 or by up-regulating pro-apoptotic protein families, most notably, the caspases. Caspases are a family of cystine proteases which serve critical roles in apoptotic and inflammatory signaling pathways. During tumorigenesis, significant loss or inactivation of lead members in the caspase family leads to impairing apoptosis induction, causing a dramatic imbalance in the growth dynamics, ultimately resulting in aberrant growth of human cancers. Recent exploitation of apoptosis pathways towards re-instating apoptosis induction via caspase re-activation has provided new molecular platforms for the development of therapeutic strategies effective against advanced prostate cancer as well as other solid tumors. This review will discuss the current cellular landscape featuring the caspase family in tumor cells and their activation via pharmacologic intervention towards optimized anti-cancer therapeutic modalities. This article is part of a Special Issue entitled “Apoptosis: Four Decades Later”. uk_UA
dc.description.sponsorship The authors wish to acknowledge Drs. Steven Schwarze, Vivek Rangnekar and Stephen Strup for useful discussions and the administrative assistance of Lorie Howard. The studies have been supported by grants from the Department of Defense (USAMRMC PC073314), the James F. Hardymon Endowment at the University of Kentucky College of Medicine and the Markey Cancer Foundation. uk_UA
dc.language.iso en uk_UA
dc.publisher Інститут експериментальної патології, онкології і радіобіології ім. Р.Є. Кавецького НАН України uk_UA
dc.relation.ispartof Experimental Oncology
dc.subject Reviews uk_UA
dc.title Caspase Control: Protagonists of Cancer Cell Apoptosis uk_UA
dc.type Article uk_UA
dc.status published earlier uk_UA


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