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New EGF‐R selective tyrosine kinase inhibitor reveals variable growth responses in prostate carcinoma cell lines PC‐3 and DU‐145
Author(s) -
Jones Helen E.,
Dutkowski Carol M.,
Barrow Denise,
Harper Maureen E.,
Wakeling Alan E.,
Nicholson Robert I.
Publication year - 1997
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19970611)71:6<1010::aid-ijc17>3.0.co;2-h
Subject(s) - autocrine signalling , cell growth , epidermal growth factor , biology , platelet derived growth factor receptor , cell culture , endocrinology , growth inhibition , tyrosine kinase inhibitor , tyrosine phosphorylation , tyrosine kinase , growth factor , microbiology and biotechnology , medicine , signal transduction , receptor , biochemistry , cancer , genetics
The effect of an EGF‐R selective tyrosine kinase inhibitor ZM252868 was evaluated on the proliferation of PC‐3 and DU‐145 prostate cancer cell lines, which are purported to utilize an EGF‐R‐mediated autocrine pathway for regulation of cell growth. Basal growth of DU‐145 cells was inhibited in a dose‐dependent manner by the inhibitor, showing a 70% reduction at 1 μM, whilst the growth of PC‐3 cells was not affected at this concentration. In the presence of 0.1 μM inhibitor, EGF and TGFα‐stimulated DU‐145 cell growth was decreased to below basal levels, while only TGFα‐stimulated PC‐3 cell growth was inhibited at a 1‐μM concentration. Any growth responses to aFGF, bFGF, KGF, IGF1 and PDGF by DU‐145 and PC‐3 cells were unaffected by the inhibitor at concentrations of 1 μM or less. Additionally, the distribution of immunoreactive EGF‐R varied between DU‐145 and PC‐3 cells, with EGF‐R being predominately located on the cell membrane and in the cytoplasm, respectively. Int. J. Cancer 71:1010‐1018, 1997. © 1997 Wiley‐Liss Inc.