Document Detail


A peptide inhibitor derived from p55PIK phosphatidylinositol 3-kinase regulatory subunit: a novel cancer therapy.
MedLine Citation:
PMID:  19074847     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
p55PIK, a regulatory subunit of phosphatidylinositol 3-kinase (PI3K), specifically interacts with retinoblastoma protein (Rb) through the unique NH2 terminus of p55PIK, N24. This interaction is critical for cell proliferation and cell cycle progression. To examine p55PIK as a potential target for cancer therapy, we generated an adenovirus expressing N24 (Ad-N24-GFP) and studied its effects on the proliferation of cultured cancer cells, including human colon (HT29) and thyroid (FTC236) cancer cells. Ad-N24-GFP blocked cell proliferation and induced cell cycle arrest in all cancer cell lines tested. N24 induced cell cycle arrest at G0-G1 phase in cell lines that expressed Rb. Interestingly, N24 inhibited cell proliferation by blocking cell cycle transition at both S and G2-M phases in FTC236 cells, which did not express Rb. When Rb was knocked down by short hairpin RNA in HT29 cells, N24 also inhibited cell cycle progression at S and G2-M phases, suggesting that p55PIK regulates cell cycle progression by Rb-dependent and Rb-independent mechanisms. Finally, Ad-N24-GFP markedly decreased the growth of xenograft tumors derived from HT29 and FTC236 cancer cells in athymic nude mice. Our data strongly suggest that N24 peptide is an effective anticancer therapy, which specifically inhibits PI3K signaling pathways mediated by p55PIK. Moreover, they show that the regulatory subunit of an enzyme, in addition to its catalytic subunit, can be an important target for drug development.
Authors:
Junbo Hu; Xianmin Xia; Aiwu Cheng; Guihua Wang; Xuelai Luo; Michael F Reed; Tito Fojo; Alexis Oetting; Jianping Gong; Paul M Yen
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Molecular cancer therapeutics     Volume:  7     ISSN:  1535-7163     ISO Abbreviation:  Mol. Cancer Ther.     Publication Date:  2008 Dec 
Date Detail:
Created Date:  2008-12-16     Completed Date:  2009-02-09     Revised Date:  2010-02-01    
Medline Journal Info:
Nlm Unique ID:  101132535     Medline TA:  Mol Cancer Ther     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3719-28     Citation Subset:  IM    
Affiliation:
Department of Surgery, Tongji Medical School, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
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MeSH Terms
Descriptor/Qualifier:
1-Phosphatidylinositol 3-Kinase / chemistry,  metabolism,  pharmacology*,  physiology*
Animals
Antineoplastic Agents / pharmacology*
Cell Line, Tumor
Enzyme Inhibitors / pharmacology
Gene Expression Regulation, Enzymologic*
Gene Expression Regulation, Neoplastic*
Humans
Male
Mice
Mice, Nude
Neoplasm Transplantation
Neoplasms / drug therapy*,  enzymology,  metabolism*,  pathology
Peptide Fragments / chemistry,  pharmacology*
Peptides / pharmacology*
Retinoblastoma Protein / metabolism
Chemical
Reg. No./Substance:
0/Antineoplastic Agents; 0/Enzyme Inhibitors; 0/N24 peptide, human; 0/Peptide Fragments; 0/Peptides; 0/Retinoblastoma Protein; EC 2.7.1.137/1-Phosphatidylinositol 3-Kinase; EC 2.7.1.137/PIK3R3 protein, human

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