Premium
Rap1‐suppressed tumorigenesis is concomitant with the interference in Ras effector signaling
Author(s) -
Lin Yea-Lih,
Mettling Clément,
Chou Chen-Kung
Publication year - 2000
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(00)01150-9
Subject(s) - rap1 , mapk/erk pathway , transfection , signal transduction , cancer research , microbiology and biotechnology , kinase , anti apoptotic ras signalling cascade , chemistry , effector , carcinogenesis , biology , cell culture , biochemistry , gene , genetics
Expression of Rap1 blocks epithelial growth factor‐induced extracellular signal‐regulated kinases (ERKs) activation. However, recent studies demonstrated that Rap1 mediates ERKs activation induced by nerve growth factor. The anti‐oncogenic effect of Rap1 has been reported but its mechanism remains unclear. To evaluate the correlation between the anti‐transforming effect and the activation of ERKs, we transfected rap1 cDNA into Hep3B cells and selected stable transfectants. The Rap1 transfectants completely lost their intrinsic tumorigenicity in Balb/c nude mice. Both insulin and 12‐ O ‐tetradecanoyl phorbol‐13‐acetate (TPA)‐stimulated ERK activations were also blocked. Our findings suggest that Rap1‐suppressed tumorigenicity is concomitant with ERKs inhibition.