Axl receptor tyrosine kinase expression in human lung cancer cell lines correlates with cellular adhesion

被引:109
作者
Wimmel, A
Glitz, D
Kraus, A
Roeder, J
Schuermann, M
机构
[1] Klinikum Univ Marburg, Klin Innere Med Sp Hamatol Onkol Immunol, D-35033 Marburg, Germany
[2] Aventis Behring GMBH, D-35041 Marburg, Germany
关键词
Axl receptor tyrosine kinase; Gas6; lung cancer; cell adhesion;
D O I
10.1016/S0959-8049(01)00271-4
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Axl is a receptor tyrosine kinase (RTK) with oncogenic potential and transforming activity, Since Axl bears structural similarities to cell adhesion molecules such as neural cell adhesion molecule (NCAM) (FNIII domains), it is thought that Axl might play a role in adhesion. In this study, we have analysed the expression of the Axl protein and its ligand, Gas6. in human lung cancer cell lines of different histological origin. Axl expression occurred in approximately 60% of non-small Cell lung cancer (NSCLC) cell lines, which grow adherently, and in normal bronchial epithelial cells (NHBE). but not ill cell lines of small cell lung cancer origin (SCLC), which grow in suspension. A number of SCLC sublines, which could be selected spontaneously or after oneogene transfection for adherent growth, all expressed Axl protein. Overexpression of Axl per se, however. did not induce ally change in the adhesion phenotype. All Axl-expressing cell lines demonstrated a membrane-bound 140 kD form, as well as a soluble 85 kD form, detectable in supernatant, of Axl-RTK. Expression or the Axl ligand Gas6 was detected in approximately 80% of all cell lines investigated. We conclude from these data that loss of Axl expression is a feature or SCLC tumour cells. Axl expression appears to be a consequence of cellular adhesion and possibly influences differentiation in human lung cancers. (C) 2001 Published by Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:2264 / 2274
页数:11
相关论文
共 31 条
[1]  
Avanzi GC, 1997, EXP HEMATOL, V25, P1219
[2]   GAS6 inhibits granulocyte adhesion to endothelial cells [J].
Avanzi, GC ;
Gallicchio, M ;
Bottarel, F ;
Gammaitoni, L ;
Cavalloni, G ;
Buonfiglio, D ;
Bragardo, M ;
Bellomo, G ;
Albano, E ;
Fantozzi, R ;
Garbarino, G ;
Varnum, B ;
Aglietta, M ;
Saglio, G ;
Dianzani, U ;
Dianzani, C .
BLOOD, 1998, 91 (07) :2334-2340
[3]   Signaling through the ARK tyrosine kinase receptor protects from apoptosis in the absence of growth stimulation [J].
Bellosta, P ;
Zhang, Q ;
Goff, SP ;
Basilico, C .
ONCOGENE, 1997, 15 (20) :2387-2397
[4]  
BELLOSTA P, 1995, MOL CELL BIOL, V15, P614
[5]   Intracellular signaling of the Ufo/Axl receptor tyrosine kinase is mediated mainly by a multi-substrate docking-site [J].
Braunger, J ;
Schleithoff, L ;
Schulz, AS ;
Kessler, H ;
Lammers, R ;
Ullrich, A ;
Bartram, CR ;
Janssen, JWG .
ONCOGENE, 1997, 14 (22) :2619-2631
[6]   Determinants for transformation induced by the Axl receptor tyrosine kinase [J].
Burchert, A ;
Attar, EC ;
McCloskey, P ;
Fridell, YWC ;
Liu, ET .
ONCOGENE, 1998, 16 (24) :3177-3187
[7]  
Carbone DP, 1997, SEMIN ONCOL, V24, P388
[8]  
Costa M, 1996, J CELL PHYSIOL, V168, P737, DOI 10.1002/(SICI)1097-4652(199609)168:3<737::AID-JCP27>3.0.CO
[9]  
2-U
[10]   New insights into the control of cell growth; The role of the Axl family [J].
Crosier, KE ;
Crosier, PS .
PATHOLOGY, 1997, 29 (02) :131-135