Links between alpha-catenin, NF-kappaB, and squamous cell carcinoma in skin.
Ontology highlight
ABSTRACT: Cancers display a diverse set of cellular defects, which are thought to be elicited by multiple genetic mutations. In this study, we show that when a single adherens junction protein, alpha-catenin, is removed by conditional targeting, the entire skin epidermis systematically transforms to a hyperproliferative, invasive tissue replete with inflammation. Transcriptional profiling and biochemical analyses reveal that alpha-catenin ablation is accompanied by activation of NF-kappaB and its proinflammatory target genes, along with genes involved in proliferation, wound healing, angiogenesis, and metastasis. Many of these alterations occur in vitro and in the embryo, and thus seem at least partly to be intrinsic to the loss of alpha-catenin. We show that reductions in alpha-catenin, activation
SUBMITTER: Kobielak A
PROVIDER: S-EPMC1413714 | biostudies-literature | 2006 Feb
REPOSITORIES: biostudies-literature
ACCESS DATA