Sphingosine inhibits attachment of murine Lewis lung carcinoma cells to laminin and type IV collagen

FEBS Letters

Jimbo, Masayuki¹  Inokuchi, Jin-ichi¹  Kumamoto, Yukihiro¹  Nagamatsu, Atsuo¹  Shimeno, Hiroshi¹ 

[1] Department of Biochemistry, Faculty of Pharmaceutical Sciences, Fukuoka University, Nanakuma 8-19-1, Jonan-ku, Fukuoka 814-01, Japan

关键词: Sphingosine;    Cell adhesion;    Protein kinase C;    Laminin;    Collagen type IV;    Lewis lung carcinoma;    SPH;    sphingosine;    3LL;    Lewis lung carcinoma;    PMA;    phorbol 12-myristate 13-acetate;    PKC;    protein kinase C;    RPMI;    Roswell Park Memorial Institute;    BSA;    bovine serum albumin;    HPF;    high power field;    D-PDMP;    D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol;   

DOI  :  10.1016/0014-5793(91)80935-V

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

The effect of sphingosine (SPH) on the adhesive properties of Lewis lung carcinoma (3LL) cells was investigated using plastic precoated with the extracellular matrix proteins, laminin, fibronectin, or type IV collagen. Treatment of 3LL cells with SPH (0.5–10 μM) resulted in a dose-dependent decrease in the ability to bind to laminin and type IV collagen but had little or no effect on atachment to fibronectin. Phorbol 12-myristate 13-acetate (PMA) selectively enhanced attachment of 3LL cells to laminin and collagen. The inhibitory effect of SPH on attachment to both proteins was competitively antagonized by PMA. These results suggest that SPH acts as a negative effector for cell attachment to laminin and collagen, and that the cell attachment process to both proteins might be regulated in part by protein kinase C.

【 授权许可】

Unknown