Relative expression of epidermal growth factor receptor in placental cytotrophoblasts and choriocarcinoma cell lines

The role of transforming growth factor-α (TGF-α)-epidermal growth factor receptor (EGFR) interactions in regulating benign and malignant trophoblast proliferation were examined. Benign cytotrophoblast (CT) demonstrated mitogenic stimulation in response to TGF-α; BeWo and JAr choriocarcinoma cell lin...

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Bibliographic Details
Published in:	Placenta (Eastbourne) Vol. 18; no. 1; pp. 17 - 27
Main Authors:	Filla, M.S., Kaul, K.L.
Format:	Journal Article
Language:	English
Published:	Oxford Elsevier Ltd 1997 Elsevier
Subjects:	Antibodies, Blocking - pharmacology Biological and medical sciences Cell Division - drug effects Choriocarcinoma - drug therapy Choriocarcinoma - metabolism Choriocarcinoma - pathology Enzyme-Linked Immunosorbent Assay Female General aspects (metabolism, cell proliferation, established cell line...) Humans Immunoenzyme Techniques Medical sciences Pregnancy Receptor Protein-Tyrosine Kinases - metabolism Receptor, Epidermal Growth Factor - analysis Receptor, Epidermal Growth Factor - biosynthesis Transforming Growth Factor alpha - immunology Transforming Growth Factor alpha - pharmacology Trophoblasts - cytology Trophoblasts - drug effects Trophoblasts - metabolism Tumor cell Tumor Cells, Cultured Tumors Human Cell proliferation Trophoblaste Fetal membrane Transforming growth factor β Malignant tumor Carcinogenesis In vitro Autocrine secretion Regulation(control) Cell line Epidermal growth factor Chorioepithelioma Biological receptor
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Summary:	The role of transforming growth factor-α (TGF-α)-epidermal growth factor receptor (EGFR) interactions in regulating benign and malignant trophoblast proliferation were examined. Benign cytotrophoblast (CT) demonstrated mitogenic stimulation in response to TGF-α; BeWo and JAr choriocarcinoma cell lines failed to respond. EGFR levels in BeWo and JAr were determined by enzyme linked immunoassay (ELISA) to be at least 10-fold higher than those in benign CT. EGFR isolated from BeWo and JAr also demonstrated functional tyrosine kinase activity. Using a combination of immunoperoxidase (IP) and ELISA techniques, choriocarcinoma cells were found to produce significant quantities of TGF-α that were comparable with those reported previously by this laboratory for benign CT, and were felt to be stimulating their own proliferation in an autocrine fashion. EGFR blocking and TGF-α neutralizing antibodies inhibited JAr proliferation whereas an EGF neutralizing antibody did not. The data presented here and in our previous report indicate that a TGF-α-EGFR autocrine loop may regulate normal and malignant CT proliferation. Choriocarcinoma cells may be proliferating at a maximal rate due, in part, to EGFR overexpression and are therefore unable to respond further to exogenous growth factor. Thus, EGFR overexpression may contribute to the uncontrolled proliferation of choriocarcinoma cells in general.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0143-4004 1532-3102
DOI:	10.1016/S0143-4004(97)90067-9