Alteration of beta-catenin expression in esophageal squamous-cell carcinoma
Authors
Ninomiya, I
Endo, Y
Fushida, S
Sasagawa, T
Miyashita, T
Fujimura, T
Nishimura, G
Tani, T
Hashimoto, T
Yagi, M
Shimizu, K
Ohta, T
Yonemura, Y
Inoue, M
Sasaki, T
Miwa, K
Citation
I. Ninomiya et al., Alteration of beta-catenin expression in esophageal squamous-cell carcinoma, INT J CANC, 85(6), 2000, pp. 757-761
Categorie Soggetti
Onconogenesis & Cancer Research
Journal title
INTERNATIONAL JOURNAL OF CANCER
SICI code
0020-7136(20000315)85:6<757:AOBEIE>2.0.ZU;2-#
Abstract
beta-catenin regulates cadherin-mediated cell-cell adhesion and also functi
ons as a signaling molecule. In this study, we examined the expression patt
ern of E-cadherin, alpha-catenin and beta-catenin in 22 cases of esophageal
squamous-cell carcinoma by Western-blot analysis. Expression of E-cadherin
, alpha-catenin and beta-catenin was lower in carcinomas than in normal eso
phageal mucosa in 4 cases(18.2%) for E-cadherin, 6 cases (27.3%) for alpha-
catenin and 9 cases (40.9%) for beta-catenin, Expression of beta-catenin wa
s not always correlated with that of E-cadherin. Over-expression of beta-ca
tenin was observed in 3 cases (13.6%). Of 3 cases that presented with over
expression of beta-catenin, 2 showed cytoplasmic staining by immunohistoche
mistry. Nuclear localization of beta-catenin was observed in one case that
had higher beta-catenin level in tumor tissue (1.4-fold higher than normal
mucosa). The genomic DNA sequences of the beta-catenin and the APC gene wer
e analyzed. No mutation of the beta-catenin gene was observed in any cases.
Silent mutation of the APC gene was found in all the cases that showed ove
r-expression or nuclear localization of the beta-catenin protein, These res
ults indicate that alterations of the cadherin-catenin complex may play an
important role in a sub-set of esophageal carcinogenesis. Furthermore, it i
s suggested that beta-catenin over expression is not caused by genetic alte
ration of either the beta-catenin or the APC gene. (C) 2000 Wiley-Liss, Inc
.