Please use this identifier to cite or link to this item: https://doi.org/10.1186/1755-8794-5-34
Title: Genetic and bioinformatic analyses of the expression and function of PI3K regulatory subunit PIK3R3 in an Asian patient gastric cancer library
Authors: Zhou, J. 
Chen, G.B.
Tang, Y.C. 
Sinha, R.A.
Wu, Y.
Yap, C.S.
Wang, G.
Hu, J.
Xia, X.
Tan, P. 
Goh, L.K. 
Yen, P.M.
Issue Date: 2012
Citation: Zhou, J., Chen, G.B., Tang, Y.C., Sinha, R.A., Wu, Y., Yap, C.S., Wang, G., Hu, J., Xia, X., Tan, P., Goh, L.K., Yen, P.M. (2012). Genetic and bioinformatic analyses of the expression and function of PI3K regulatory subunit PIK3R3 in an Asian patient gastric cancer library. BMC Medical Genomics 5 : -. ScholarBank@NUS Repository. https://doi.org/10.1186/1755-8794-5-34
Abstract: Background: While there is strong evidence for phosphatidylinositol 3-kinase (PI3K) involvement in cancer development, there is limited information about the role of PI3K regulatory subunits. PIK3R3, the gene that encodes the PI3K regulatory subunit p55, is over-expressed in glioblastoma and ovarian cancers, but its expression in gastric cancer (GC) is not known. We thus used genetic and bioinformatic approaches to examine PIK3R3 expression and function in GC, the second leading cause of cancer mortality world-wide and highly prevalent among Asians. Methods. Primary GC and matched non-neoplastic mucosa tissue specimens from a unique Asian patient gastric cancer library were comprehensively profiled with platforms that measured genome-wide mRNA expression, DNA copy number variation, and DNA methylation status. Function of PIK3R3 was predicted by IPA pathway analysis of co-regulated genes with PIK3R3, and further investigated by siRNA knockdown studies. Cell proliferation was estimated by crystal violet dye elution and BrdU incorporation assay. Cell cycle distribution was analysed by FACS. Results: PIK3R3 was significantly up-regulated in GC specimens (n=126, p
Source Title: BMC Medical Genomics
URI: http://scholarbank.nus.edu.sg/handle/10635/110545
ISSN: 17558794
DOI: 10.1186/1755-8794-5-34
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