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Accession Number ADA570124
Title Metabolic Regulation of Ovarian Cancer Cell Death.
Publication Date Jul 2012
Media Count 7p
Personal Author S. Kornbluth
Abstract Following treatment with chemotherapeutic agents, responsive ovarian cancer cells undergo apoptotic cell death. Several groups have shown that the apoptotic protease, caspase 2 (C2), is an essential activator of cell death in ovarian cancer cells treated with cisplatin and we have found, by knock-down of C2 in ovarian cancer cells, that C2 is also required for responsiveness to microtubule-perturbing agents such as paclitaxel. Work from our laboratory has demonstrated that C2 is normally controlled by the metabolic status of the cell in that high levels of flux through the pentose phosphate pathway (PPP) prevents activation of C2. Because ovarian cancers exhibit increased glucose uptake and increased fatty acid synthesis, we hypothesized that susceptibility of ovarian cancers to front-line chemotherapeutic agents, reflect, at least in part, the metabolic status of the cells and, consequently, the phosphorylation state of caspase 2. In this past year, we have found that fatty acid synthesis inhibition kills ovarian cancer cells through the induction of a protein known as REDDI. REDDI induction leads to (and is required for) caspase 2 activation, leading to death of the cells.
Keywords Activation
Chemotherapeutic agents
Fatty acids
Ovarian cancer
Peptide hydrolases

Source Agency Non Paid ADAS
NTIS Subject Category 57A - Anatomy
57S - Physiology
57E - Clinical Medicine
Corporate Author Duke Univ., Durham, NC.
Document Type Technical report
Title Note Final rept. 1 Jul 2011-30 Jun 2012.
NTIS Issue Number 1314
Contract Number W81XWH-10-1-0344

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