Inhibition of 3H-TdR uptake for human gastric carcinoma cells by epidermal growth factor specific antibody.
This study examined whether human gastric carcinoma cells produced EGF for self-stimulation, using TMK-1 and MKN-28 cells which express mRNA for EGF and EGF receptor. EGF protein production was confirmed by ELISA and flow cytometric analysis. The lysates of these cells replaced EGF-induced biological activity to EGF receptor bearing KB cells but the culture supernatants did not. Furthermore, EGF-radioreceptor assay revealed non-secretion of EGF product. EGF specific monoclonal antibody neutralized exogenous EGF-induced 3H-TdR uptake, and inhibited spontaneous 3H-TdR uptake of TMK-1 and MKN-28 cells. These results suggest that EGF specific antibody binds to EGF protein at the cell surface, leading to the inhibition of 3H-TdR uptake, and that EGF produced by tumor cells may act as an autocrine growth factor in human gastric carcinoma cells.
Kyo
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First Department of Pathology, Hiroshima University School of Medicine, Japan.
D000911:Antibodies, Monoclonal; D004815:Epidermal Growth Factor / Q000037:antagonists & inhibitors / Q000096:biosynthesis*; D066246:ErbB Receptors / Q000378:metabolism; D006801:Humans; D012333:RNA, Messenger / Q000378:metabolism; D013936:Thymidine / Q000378:metabolism; D014407:Tumor Cells, Cultured / Q000378:metabolism*
D000911:Antibodies, Monoclonal; D012333:RNA, Messenger; D004815:Epidermal Growth Factor; D066246:ErbB Receptors; D013936:Thymidine