Rap1‐suppressed tumorigenesis is concomitant with the interference in Ras effector signaling

FEBS Letters

Mettling, Clément¹  Chou, Chen-Kung²  Lin, Yea-Lih¹ 

[1] Institut de Génétique Humaine, Centre National de la Recherche Scientifique, 141 rue de la Cardonille, 34396 Montpellier Cedex 5, France;Department of Medical Research, Veterans General Hospital, Shih-Pai, Taipei, Taiwan

关键词: Rap1;    Extracellular signal-regulated kinase;    GTPase;    Mitogenesis;    Insulin;    12-O-Tetradecanoyl phorbol-13-acetate;    ERK;    extracellular signal-regulated kinase;    MEK;    mitogen-activated/extracellular signal-regulated kinase kinase;    IRS;    insulin receptor substrate;    TPA;    12-O-tetradecanoyl phorbol-13-acetate;    GEF;    guanylnucleotide exchange factor;   

DOI  :  10.1016/S0014-5793(00)01150-9

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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.

【 授权许可】

Unknown