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Change in metabolic turnover is an alternate mechanism increasing cell surface epidermal growth factor receptor levels in tumor cells.

Gamou, S, Shimizu, N·1987·Journal of Biological Chemistry
DOI 10.1016/s0021-9258(18)48300-7
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Abstract

The biosynthesis and metabolic turnover of the epidermal growth factor (EGF) receptor was examined in a human pancreatic carcinoma cell line, UCVA-1. This cell line has been shown to possess a much higher level of EGF receptors than is expected solely from receptor gene/mRNA dosage. Analysis of the biosynthesis using metabolic labeling, immunological quantitation, and inhibitor treatment revealed that the naked EGF receptor in UCVA-1 cells is a protein of Mr 130,000 that is matured consecutively as a Mr 160,000 and 170,000 glycoprotein through post-translational glycosylation. Analysis of the metabolic turnover using pulse-chase labeling and inhibitor treatment revealed that the rate of EGF receptor synthesis in UCVA-1 cells was similar to that in two squamous cell carcinoma cell lines, NA and Ca9-22, which also have high numbers of EGF receptors, but because of gene amplification. In contrast, the rate of receptor degradation in UCVA-1 cells was significantly slower than in the other two cell lines. These results suggest that the retarded metabolic turnover may constitute a unique mechanism for elevating cell surface EGF receptor levels in some tumor cells independent of gene amplification.

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Crossref · 10.1016/s0021-9258(18)48300-7

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  • The increase in radiolabel during the 4-h chase in control cells is consistent with EGFR becoming more antibody reactive as the receptor undergoes posttranslational modification.

    “The increase in radiolabel during the 4-h chase in control cells (Fig. 5C) is consistent with the EGFR becoming more antibody reactive as the receptor undergoes posttranslational modification, as shown previously (65, 66).”

    From EHD1 and RUSC2 Control Basal Epidermal Growth Factor Receptor Cell Surface Expression and Recycling (2020) · cites this paper as [66]

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Metadata

Authors
Gamou, S., & Shimizu, N.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
1987-05
Volume
262
Issue
14
Pages
6708-6713
ISSN
0021-9258
DOI
10.1016/s0021-9258(18)48300-7
Cited by
27
References
0
Language
en
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