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Comparison of phosphatidylinositol‐3‐kinase signalling within a panel of human colorectal cancer cell lines with mutant or wild‐type PIK3CA
Author(s) -
Morrow Christopher J.,
Gray Alexander,
Dive Caroline
Publication year - 2005
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2005.07.096
Subject(s) - phosphatidylinositol , p110α , mutant , kinase , cell growth , biology , cell culture , microbiology and biotechnology , cancer research , gene , genetics
Recent studies have identified conserved missense mutations in PIK3CA, the gene encoding the catalytic phosphatidylinositol‐3‐kinase subunit p110α, 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.