Decreased mitogenic response to epidermal growth factor in human squamous cell carcinoma lines overexpressing epidermal growth factor receptor owing to limiting amounts of the adaptor protein Grb2: rescue by retinoic acid treatment.

Abstract:

:Growth factor receptors of the tyrosine kinase family regulate proliferation of a variety of cell types. In some human cancers, the epidermal growth factor receptor (EGFR) and its ligands often are overexpressed, leading to both constitutive and autocrine activation. Intracellular signaling via this receptor takes place through several mechanisms of action, including activation of ras and the mitogen-activated protein kinase (MAPK) pathway. Our previous studies have shown that human squamous cell carcinoma (SCC) lines overexpress EGFR and do not increase proliferation in response to exogenous epidermal growth factor (EGF). The vitamin A metabolite retinoic acid (RA) has been used as a chemotherapeutic drug in the treatment of SCC. RA decreases proliferation of SCC lines, in part owing to inhibition of EGFR expression. However, we previously found that treatment of SCC lines with inhibitory doses of RA sensitized cells to the proliferative effects of EGF. We now present a mechanism of action for this effect. RA inhibited expression of EGFR and proteins in the MAPK signaling pathway. Expression of these molecules returned to basal levels within 24 h after RA withdrawal. RA also inhibited autocrine secretion of EGF, which returned to basal levels with slower kinetics. During this time, addition of exogenous EGF stimulated mitosis in SCC lines. These data suggested that signaling proteins downstream of overexpressed EGFR may have limited the mitotic response in SCC lines. In support of this hypothesis, overexpression of the EGFR adaptor protein Grb2 increased cell proliferation and restored EGF-induced mitosis.

journal_name

Mol Carcinog

journal_title

Molecular carcinogenesis

authors

Crowe DL,Tsang KJ

doi

10.1002/mc.10011

subject

Has Abstract

pub_date

2001-12-01 00:00:00

pages

187-94

issue

4

eissn

0899-1987

issn

1098-2744

pii

10.1002/mc.10011

journal_volume

32

pub_type

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