| Literature DB >> 21041624 |
Feng Su1, Kathy R Kozak, Satoshi Imaizumi, Feng Gao, Malaika W Amneus, Victor Grijalva, Carey Ng, Alan Wagner, Greg Hough, Gina Farias-Eisner, G M Anantharamaiah, Brian J Van Lenten, Mohamad Navab, Alan M Fogelman, Srinivasa T Reddy, Robin Farias-Eisner.
Abstract
We examined whether reduced levels of Apolipoprotein A-I (apoA-I) in ovarian cancer patients are causal in ovarian cancer in a mouse model. Mice expressing a human apoA-I transgene had (i) increased survival (P < 0.0001) and (ii) decreased tumor development (P < 0.01), when compared with littermates, following injection of mouse ovarian epithelial papillary serous adenocarcinoma cells (ID-8 cells). ApoA-I mimetic peptides reduced viability and proliferation of ID8 cells and cis-platinum-resistant human ovarian cancer cells, and decreased ID-8 cell-mediated tumor burden in C57BL/6J mice when administered subcutaneously or orally. Serum levels of lysophosphatidic acid, a well-characterized modulator of tumor cell proliferation, were significantly reduced (>50% compared with control mice, P < 0.05) in mice that received apoA-I mimetic peptides (administered either subcutaneously or orally), suggesting that binding and removal of lysophosphatidic acid is a potential mechanism for the inhibition of tumor development by apoA-I mimetic peptides, which may serve as a previously unexplored class of anticancer agents.Entities:
Mesh：
Substances：
Year: 2010 PMID： 21041624 PMCID： PMC2993420 DOI： 10.1073/pnas.1009010107
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN： 0027-8424 Impact factor: 11.205