Open AccessMonoclonal antibodies to early pregnancy factor perturb tumour cell growth
Author(s) -
QUINN K. A.,
ATHANASASPLATSIS S.,
WONG T.Y.,
ROLFE B.E.,
CAVANAGH A. C.,
MORTON H.
Publication year - 1990
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1990.tb06448.x
Subject(s) - autocrine signalling , biology , monoclonal antibody , cell growth , immunology , cell culture , germ cell , antibody , growth factor , monoclonal , concanavalin a , cell division , cell , cancer research , in vitro , receptor , biochemistry , genetics , gene
SUMMARY The pregnancy‐associated substance early pregnancy factor (EPF) has previously been reported as a product of tumours of germ cell origin. More recently EPF (or an EPF‐related substance, tEPF) has also been detected in the serum of patients bearing tumours of non‐germ cell origin. We report here the production of tEPF by a variety of cultured transformed and tumour cell lines, of both germ and non‐germ cell origin. Antibodies specific for EPF remove all tEPF activity from tumour cell conditioned medium, tEPF production is found to be associated with cell division; tEPF is no longer detected after growth arrest or differentiation. Co‐culture of tumour cells with increasing doses of anti‐EPF monoclonal antibodies resulted in a significant, dose‐dependent decrease in rate of cell growth and viability. Similar anti‐EPF concentrations had no effect on the concanavalin A induced proliferation of mouse spleen cells. These studies suggest, therefore, that tEPF is a growth‐regulated product of cultured tumour and transformed cells. These cells are also dependent upon tEPF for continued growth, i.e. tEPF is acting in the autocrine mode.