| Literature DB >> 10446956 |
Y Nagasawa1, Y Miyoshi, K Iwao, Y Shinomura, Y Matsuzawa, Y Nakamura.
Abstract
To shed light on the oncogenic nature of mutant beta-catenin, we introduced a form of the cDNA that lacked an entire exon 3 into L cells derived from murine s.c. tissue. Aberrant beta-catenin protein accumulated in the cytoplasm and nuclei of these cells (designated L-MT), whereas in L cells transfected with wild-type beta-catenin (designated L-N), normal beta-catenin protein was expressed at a level similar to that of parental cells. L-MT cells also changed morphologically from a fibroblast-like appearance to a more cuboidal shape. Their rate of proliferation was the same as that of L cells and L-N cells, but the saturation density of L-MT cells appeared to increase in association with a multilayer growth pattern. Furthermore, L-MT cells required a lower concentration of serum in the growth medium than did parental cells. These alterations in cell growth and morphology suggested that mutated beta-catenin was stabilized in the transfected cells and induced the oncogenic phenotype.Entities:
Mesh:
Substances:
Year: 1999 PMID: 10446956
Source DB: PubMed Journal: Cancer Res ISSN: 0008-5472 Impact factor: 12.701