Profile of epidermal growth factor receptor (EGFr) expression in human malignancies: Effects of exposure to EGF and its biological influence on established human tumour cell lines
Ame. Nouri et al., Profile of epidermal growth factor receptor (EGFr) expression in human malignancies: Effects of exposure to EGF and its biological influence on established human tumour cell lines, INT J MOL M, 6(4), 2000, pp. 495-500
The aim of this study was to compare the profile of EGFr expression in tran
sitional cell carcinoma of the bladder (TCC) and in oral squamous cell carc
inoma (OSCC). In addition, to study the influence of EGF stimulation on the
expression of major histocompatibility complex class I antigens, placental
alkaline phosphatase (PLAP) as well as changes in tumour cell sensitivity
to cisplatin using immunocytochemical staining, a colorimetric assay and SD
S-gel electrophoresis. The results showed that: a) strong EGFr expression c
ould be seen in 22/88 (27%) cases of TCCs. In oral tumours the values for n
on-invasive ameloblastoma and invasive OSCC were 4/25 (16%) and 30/41 (73%)
respectively. b) EGFr expression in tumour cell lines paralleled that of t
umour biopsies. The number of lines expressing high and low EGFr expression
amongst TCCs were 4 and 4 and in OSCCs were 3 and 1 respectively. c) Expos
ure of tumour cell lines to EGF led to: i) an increase in EGFr expression (
stimulatory indices SI, ranged from 1.06 to 2.58) for TCCs but a decrease i
n the case of OSCCs (SI ranged from 0.01 to 0.85). The corresponding SI val
ues for class I antigens were 0.95-1.16 and 0.10-0.84. ii) A significant re
duction in expression of FLAP by OSCC cell lines. iii) An increased suscept
ibility of OSCC cell lines to cisplatin by as much as 14% (p<0.001). These
data demonstrated the overexpression of EGFr in a significant proportion of
TCCs. As for oral tumours it depended on whether they were of an invasive
or non-invasive type. In the invasive cases the majority overexpressed EGFr
. The exposure of OSCC but not TCC tumour cells to EGF resulted in down reg
ulation of EGFr and class I antigens. The expression of FLAP was also signi
ficantly reduced. Exposure of OSCC cells to EGF resulted in their increased
susceptibility to cisplatin. The data supports the notion that the mitogen
ic activation of some tumour cells by EGF resulted in a reduction of their
immune visibility, differentiation status and an increase in chemosensitivi
ty.