Beta-catenin/LEF-1 induced epithelial-mesenchymal transition in DLD1 colon carcinoma cells
Ontology highlight
ABSTRACT: Our goal was to assess gene expression changes that occur when Lymphoid Enhancer Factor-1 (LEF-1) promotes epithelial-mesenchymal transition (EMT), the primary mechanism of tumor metastasis. To observe this phenomenon without interference from other signaling pathways, we selected DLD1 colon carcinoma cells (ATCC) which contain a mutation in APC. APC is a necessary component of a ubiquitin protein complex (including GSK-3beta, Axin, etc.) that is responsible for degrading cytoplasmic beta-catenin. Therefore, sufficient levels of LEF-1 can be easily activated by forming complexes with the abundant beta-catenin located in the cytoplasm of DLD1 cells. These complexes can then promote transcription of genes that stimulate EMT. We treated DLD1 cells with an adenoviral LEF-1 expression construct, which induced EMT within 48 hours. RNA was then extracted from these cells along with untreated DLD1 cells, then subjected to microarray analysis. From this analysis, we acquired several gene expression profiles by which epithelial colon carcinoma cells transform to an invasive, mesenchymal phenotype to initiate metastasis. Keywords: epithelial-mesenchymal transition, tumor metastasis, cancer progression, epithelial cell plasticity
ORGANISM(S): Homo sapiens
PROVIDER: GSE3229 | GEO | 2006/06/01
SECONDARY ACCESSION(S): PRJNA92757
REPOSITORIES: GEO
ACCESS DATA