Please use this identifier to cite or link to this item:
Title: PI3K stimulates DNA synthesis and cell-cycle progression via its p55PIK regulatory subunit interaction with PCNA
Authors: Wang, G.
Cao, X.
Lai, S.
Luo, X.
Feng, Y.
Xia, X.
Yen, P.M. 
Gong, J.
Hu, J.
Issue Date: Oct-2013
Citation: Wang, G., Cao, X., Lai, S., Luo, X., Feng, Y., Xia, X., Yen, P.M., Gong, J., Hu, J. (2013-10). PI3K stimulates DNA synthesis and cell-cycle progression via its p55PIK regulatory subunit interaction with PCNA. Molecular Cancer Therapeutics 12 (10) : 2100-2109. ScholarBank@NUS Repository.
Abstract: Previously, we have shown that p55PIK, an isoform of class IA phosphoinositide 3-kinase (PI3K), specifically interacts with important cell-cycle regulators, such as retinoblastoma (Rb), to promote cellcycle progression. Here, we used the glutathione S-transferase pull-down assay to identify other p55PIKinteracting proteins besides Rb in a Rb-deficient cell line and found that p55PIK interacted with proliferation cell nuclear antigen (PCNA), which plays a key role in coordinating both initiation of the leading strand DNA replication and discontinuous lagging strand synthesis. Overexpression of p55PIK increased, and knockdown decreased, DNA synthesis and DNA replication by modulating the binding of DNA polymerase d (Pold) to PCNA. Moreover, a cell-permeable peptide containing the N-terminal- binding domain of p55PIK (TAT-N24) disrupted the p55PIK-PCNA interaction in cancer cells, and also inhibited the DNA synthesis and tumor growth in cell culture and in vivo. Altogether, our results show that the p55PIK-PCNA interaction is important in regulating DNA synthesis and contributes to tumorigenesis. Furthermore, the p55PIK-PCNA interaction provides a potential new target for anticancer drug development. © 2013 AACR.
Source Title: Molecular Cancer Therapeutics
ISSN: 15357163
DOI: 10.1158/1535-7163.MCT-12-0920
Appears in Collections:Staff Publications

Show full item record
Files in This Item:
There are no files associated with this item.


checked on Jul 21, 2021


checked on Jul 21, 2021

Page view(s)

checked on Jul 11, 2021

Google ScholarTM



Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.