1.
FEBS Lett
; 587(16): 2698-704, 2013 Aug 19.
Artículo
en Inglés
| MEDLINE
| ID: mdl-23856463
RESUMEN
The cell surface glycoprotein CD44 enhances phorbol-12-myristate 13-acetate (TPA)-induced expression of p21WAF1 by stabilizing its mRNA and enhancing the protein's half-life in several cell lines. Only the plasma membrane-anchored cytoplasmic tail of CD44 and its interacting ezrin, radixin, moesin (ERM) proteins are required for this effect. A mitogen activated kinase (MEK) inhibitor abolishes the action of CD44 on p21. Down-regulation of p21 dramatically decreased anchorage-independence of a cancer cell line, whereas CD44 expression in this background could partially rescue the phenotype.