Premium
Two newly established cell lines derived from the same colonic adenocarcinoma exhibit differences in EGF‐receptor ligand and adhesion molecule expression
Author(s) -
Solic Nicola,
Collins Jane E.,
Richter Audrey,
Holt Susan J.,
Campbell Ian,
Alexander Peter,
Davies Donna E.
Publication year - 1995
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/ijc.2910620111
Subject(s) - epidermal growth factor , amphiregulin , biology , receptor , cell culture , cell adhesion molecule , transforming growth factor , growth factor , tgf alpha , northern blot , integrin , microbiology and biotechnology , messenger rna , genetics , gene
Two morphologically distinct cell lines, GP2d and GP5d, derived from the same adenocarcinoma of the colon, have been established and characterised. Both clones have the same genetic changes, consistent with the usual pattern of tumour progression in colon cancer. The cells also have an inverted duplication of bands 10q11 to 10q21, but Southern blot analysis failed to identify any translocations involving the ret protooncogene, which maps to this region. GP2d grew by spreading from the edges of microcolonies to form a confluent layer of cells. GP5d grew in discrete islands of cells forming multilayered colonies. These differing patterns of growth correlated with variation in expression or cellular distribution of α 2 ‐integrin, desmoplakin and e‐cadherin. Only GP2d responded to exogenously added epidermal growth factor (EGF), transforming growth factor‐alpha (TGFα) or insulin with an increase in cell numbers, even though both cell lines possessed similar numbers of EGF receptors. Analysis of EGF receptor ligand expression showed that GP5d cells expressed relatively more TGFα mRNA than did GP2d; in contrast, amphiregulin mRNA, which was abundant in GP2d, was virtually undetectable in GP5d. Even though GP5d failed to exhibit a growth response to EGF, it underwent a marked epithelial‐mesenchymal transition when treated with EGF, indicating separation of growth and morphological responses to EGF. © 1995 Wiley‐Liss Inc.