J.Jpn. Surg. Soc.
ISSN 1880-1129

[Abstract] [Full Text PDF] （in Japanese / 2006KB） [Members Only And Two Factor Auth.]

J.Jpn. Surg. Soc.. 99(7): 402-408, 1998

Feature topic

DYSFUNCTION OF E-CADIHERIN-CATENIN SYSTEM IN INVASION AND METASTASIS OF COLORECTAL CANCER

1) Pathology Division, National Cancer Center Research Institute, Tokyo, Japan
2) Second Deprtment of Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan

Keiji Maruyama1)2), Atsushi Ochiai1), Satoshi Nakamura2), Shozo Baba2), Setsuo Hirohashi1)

The E-cadherin-mediated cell adhesion system is now considered to be an “invasion suppressor system” in cancer cells. Dysfunction of the E-cadherin system due to mutations of the genes of E-cadherin and catenins has not been reported in colorectal cancer. Histologically, well-differentiated colorectal cancer cells are found to be scattered at the invasive front in primary lesions and form glands again in metastatic sites. We have reported the association and presence of signal transduction between c-erbB-2/epidermal growth factor receptor (EGF-R) and β-catenin in human cancer cells. This temporal dysfunction of the E-cadherin system observed in colon cancers may be caused by tyrosine phosphorylation of 3-catenin through activated receptortype tyrosine kinases. Overexpression of EGF-R and tyrosine phosphorylation of β-catenin are often observed in ‘‘focal dedifferentiated cells” at the invasive front of colorectal cancers. In addition, β-catenin expression is regulated by the APC tumor suppressor gene product. Thus the E-cadherin-catenin system may play important roles not only in invasion and metastasis but also in the carcinogenesis of colorectal cancer.

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