Comparison of phosphatidylinositol-3-kinase signalling within a panel of human colorectal cancer cell lines with mutant or wild-type PIK3CA |
| |
Authors: | Morrow Christopher J Gray Alexander Dive Caroline |
| |
Affiliation: | Cellular and Molecular Pharmacology Group, Paterson Institute for Cancer Research, Christie Hospital NHS Trust, Wilmslow Road, Withington, Manchester M20 4BX, United Kingdom. |
| |
Abstract: | Recent studies have identified conserved missense mutations in PIK3CA, the gene encoding the catalytic phosphatidylinositol-3-kinase subunit p110alpha, in a variety of human cancers. Further investigation demonstrated that PIK3CA mutations lead to increased basal phosphatidylinositol-3-kinase activity, promoting cell growth and invasion [Samuels, Y., Diaz, L.A., Jr., Schmidt-Kittler, O., Cummins, J.M., Delong, L., Cheong, I., Rago, C., Huso, D.L., Lengauer, C., Kinzler, K.W., Vogelstein, B. and Velculescu, V.E. (2005) Mutant PIK3CA promotes cell growth and invasion of human cancer cells. Cancer Cell 7, 561-573]. A panel of commonly used colorectal cancer cell lines was screened for these PIK3CA mutations. Constitutive and IGF-1-stimulated phosphatidylinositol-3-kinase activity, signal response and duration were assessed. In the assays used no differences distinguished cells carrying PIK3CA mutations indicating that these mutations did not significantly alter growth factor stimulated or steady state phosphatidylinositol-3-kinase activity in normal cell culture conditions. |
| |
Keywords: | PI3-K, phosphatidylinositol-3-kinase IGF-1, insulin-like growth factor1 RTK, receptor tyrosine kinase PtdIns(4,5)P2, phosphatidylinositol(4,5)bisphosphate PtdIns(3,4,5)P3, phosphatidylinositol(3,4,5)triphosphate PKB, protein kinase B PTEN, phosphatase and tensin homologue deleted on chromosome 10 MIN, micro-satellite instability CRC, colorectal cancer S.E.M., standard error of the mean |
本文献已被 ScienceDirect PubMed 等数据库收录! |
|