Open AccessAnalysis of the β‐Catenin/T Cell Factor Signaling Pathway in 36 Gastrointestinal and Liver Cancer Cells
Author(s) -
Ikenoue Tsuneo,
Ijichi Hideaki,
Kato Naoya,
Kanai Fumihiko,
Masaki Tsutomu,
Rengifo William,
Okamoto Makoto,
Matsumura Masayuki,
Kawabe Takao,
Shiratori Yasushi,
Omata Masao
Publication year - 2002
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.2002.tb01226.x
Subject(s) - beta catenin , cancer research , adenomatous polyposis coli , signal transduction , cancer , cell culture , downregulation and upregulation , colorectal cancer , wnt signaling pathway , cell , biology , medicine , microbiology and biotechnology , genetics , gene
We investigated the frequency and mechanism of |bT‐catenin/T cell factor (Tcf) signaling activation in a panel of 36 human gastrointestinal and liver cancer cell lines. Reporter assay and electrophoretic mobility shift assay revealed that the β‐catenin/Tcf signaling was upregulated in 12 of 12 (100%) colorectal, 5 of 8 (68%) gastric, 2 of 7 (29%) hepatic, and none of 9 pancreatic cancer cell lines. The activation of the pathway was mainly due to the mutation of adenomatous polyposis coli (APC) or β‐catenin, and Tcf‐4 was highly expressed in these cell lines with upregulated signaling. Nuclear β‐catenin was observed not only in the signaling‐activated cell lines, but also in 14 of 25 (56%) primary gastric cancers, 15 of 20 (75%) colon cancers, 5 of 19 (26%) hepatocellular carcinomas, and none of 13 pancreatic cancers. The presence of signaling‐upregulated gastric cancer cell lines with intact APC and β‐catenin suggests the involvement of other mechanisms than mutations of APC or β‐catenin.