Epidermal-Growth-Factor-Dependent Transformation by a Human EGF Receptor Proto-Oncogene

Abstract

The epidermal growth factor (EGF) receptor gene EGFR has been placed in a retrovirus vector to examine the growth properties of cells that experimentally overproduce a full-length EGF receptor. NIH 3T3 cells transfected with the viral DNA or infected with the corresponding rescued retrovirus developed a fully transformed phenotype in vitro that required both functional EGFR expression and the presence of EGF in the growth medium. Cells expressing 4 x 10(5) EGF receptors formed tumors in nude mice, while control cells did not. Therefore, the EGFR retrovirus, which had a titer on NIH 3T3 cells that was greater than 10(7) focus-forming units per milliliter, can efficiently transfer and express this gene, and increased numbers of EGF receptors can contribute to the transformed phenotype.

Inositol 1,4,5-Trisphosphate-independent Ca2+Mobilization Triggered by a Lipid Factor Isolated from Vitreous Body

“…The activity was followed along the purification procedure by a [Ca 2ϩ ] i mobilization bioassay as described (12). Cell Culture-Although most of the cell lines tested were able to respond to this factor (11), all the experiments were carried out on the EGFR-T17 cell line, a clone of NIH3T3 (14). To measure the biological responses, cells were seeded in 100-mm dishes and cultured to 80% confluence for 2 days in Dulbecco's modified Eagle's medium supplemented with 10% (v/v) fetal calf serum.…”

Growth inhibition of breast cancer cells by Grb2 downregulation is correlated with inactivation of mitogen-activated protein kinase in EGFR, but not in ErbB2, cells

“…Increased expression of EGFR or ErbB2 has been associated with poor survival prognosis in breast cancer patients (Koenders et al, 1992;Slamon et al, 1987). This is probably related to the association of EGFR and ErbB2 with increased cell growth (Cance and Liu, 1995;Chrysogelos and Dickson, 1994;Di Fiore et al, 1987;Ennis et al, 1989;Fitzpatrick et al, 1984;Hudziak et al, 1987;Velu et al, 1987), enhanced metastatic potential (Tan et al, 1997) and, in some cases, increased resistance to hormonal or chemotherapy (Cance and Liu, 1995;Nicholson et al, 1988;Pietras et al, 1995;Yu et al, 1996).…”

Growth inhibition of human lung adenocarcinoma cells by antibodies against epidermal growth factor receptor and by ganglioside GM3: involvement of receptor-directed protein tyrosine phosphatase(s)

“…A relation between the EGF/EGFR system and malignant cell transformation has been well established in experimental systems (Downward et al, 1984;Hayman et al, 1985;Derynck et al, 1987;Di Fiore et al, 1987;Velu et al, 1987). More importantly, EGFR expression in human breast tumours has been correlated with a poor prognosis (Perez et al, 1984;Sainsbury et al, 1985;Received 17April 1996Revised 7 August 1996 Accepted 8 August 1996 Correspondence to: R Perez and F-D Bohmer Macias et al, 1986Macias et al, , 1987aKlijn et al, 1992), and a link between EGFR activity and the malignant process has also been suggested for a number of other epithelial tumours, including non-small-cell lung cancer (NSCLC) (Khazaie et al, 1993;Modjtahedi and Dean, 1994;Fontanini et al, 1995).…”