Characterization of the influence of anti-hormone and/or anti-growth factor neutralizing antibodies on cell clone architecture and the growth of human neoplastic astrocytic cell lines.
The influence of five anti-hormone and/or anti-growth factor neutralizing antibodies on the in vitro proliferation of four human astrocytic tumor cell lines (U87, U138, U373, H4) is quantitatively described by means of a new tool which makes it possible to evaluate cell growth and cell clone architecture concomitantly. This tool relies upon the combined use of the digital cell image analyses of Feulgen-stained nuclei and the Delaunay and Voronoi mathematical triangulation and paving techniques. Of the five anti-hormone and/or anti-growth factors tested here, the anti-luteinizing hormone-releasing hormone (LHRH) antibody induced the most marked perturbation in the U138 and U373 cell lines, whereas this role was played by the anti-epidermal growth factor (EGF) antibody in the U87 and H4 cell lines. The anti-gastrin (G) antibody significantly modified the growth and/or cell clone architecture of the U138, U87 and H4 cell lines, as did the anti-transforming growth factor alpha (TGFalpha) antibody. The anti-transforming growth factor beta (TGFbeta) antibody modified the growth and/or cell clone architecture of the four cell lines under study. If the five antibodies are taken into consideration, the results strongly suggest that four (the anti-G, the anti-EGF, the anti-LHRH and the anti-TGFalpha) act as inhibitory agents on some glioma cell line proliferation, while the fifth one, i.e. the anti-TGFbeta, act as a stimulator of cell proliferation, perhaps by abrogating the inhibitory effects of TGFbeta on proliferation. A comparison of cell growth data with cell clone architecture characteristics provided further evidence of some specific influence exercised by a given hormone and/or growth factor on glioma cell proliferation. Indeed, the anti-LHRH antibody caused the most pronounced perturbations in the U138 and U373 cell clone architecture; this feature was observed in the H4 cell line and, to a lesser extent in the U87 one after the anti-EGF antibody had been used.
Camby
I
I
Laboratoire d'Histologie, Faculté de Médecine, Université Libre de Bruxelles, Belgium.
Salmon
I
I
Rorive
S
S
Gras
T
T
Darro
F
F
Kruczynski
A
A
Danguy
A
A
Pasteels
J L
JL
Kiss
R
R
D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D002455:Cell Division / Q000187:drug effects; D004815:Epidermal Growth Factor / Q000276:immunology; D005755:Gastrins / Q000276:immunology; D005909:Glioblastoma / Q000473:pathology*; D007987:Gonadotropin-Releasing Hormone / Q000276:immunology; D006801:Humans; D009447:Neuroblastoma / Q000473:pathology*; D016211:Transforming Growth Factor alpha / Q000276:immunology; D016212:Transforming Growth Factor beta / Q000276:immunology; D014407:Tumor Cells, Cultured
D000911:Antibodies, Monoclonal; D005755:Gastrins; D016211:Transforming Growth Factor alpha; D016212:Transforming Growth Factor beta; D007987:Gonadotropin-Releasing Hormone; D004815:Epidermal Growth Factor