Homodimeric galectin-7 (p53-induced gene 1) is a negative growth regulator for human neuroblastoma cells

被引:138
作者
Kopitz, J
André, S
von Reitzenstein, C
Versluis, K
Kaltner, H
Pieters, RJ
Wasano, K
Kuwabara, I
Liu, FT
Cantz, M
Heck, AJR
Gabius, HJ
机构
[1] Univ Heidelberg Klinikum, Inst Mol Pathol, D-69120 Heidelberg, Germany
[2] Univ Munich, Tierarztliche Fak, Inst Physiol Chem, D-80539 Munich, Germany
[3] Univ Utrecht, Bijvoet Ctr Biomol Res, Dept Biomol Mass Spectrometry, NL-3584 CA Utrecht, Netherlands
[4] Univ Utrecht, Utrecht Inst Pharmaceut Sci, NL-3584 CA Utrecht, Netherlands
[5] Univ Utrecht, Utrecht Inst Pharmaceut Sci, Dept Med Chem, NL-3508 TB Utrecht, Netherlands
[6] Kyushu Univ, Fac Med, Dept Anat & Cell Biol, Fukuoka 8120054, Japan
[7] Univ Calif Davis, Sch Med, Dept Dermatol, Sacramento, CA 95817 USA
关键词
apoptosis; cell growth; galectin; ganglioside; mass spectrometry; neuroblastoma;
D O I
10.1038/sj.onc.1206631
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The extracellular functions of galectin-7 (p53-induced gene 1) are largely unknown. On the surface of neuroblastoma cells (SK-N-MC), the increased GM(1) density, a result of upregulated ganglioside sialidase activity, is a key factor for the switch from proliferation to differentiation. We show by solid-phase and cell assays that the sugar chain of this ganglioside is a ligand for galectin-7. In serum-supplemented proliferation assays, galectin-7 reduced neuroblastoma cell growth without the appearance of features characteristic for classical apoptosis. The presence of galectin-3 blocked this effect, which mechanistically resembles that of galectin-1. By virtue of carbohydrate binding, galectin-7 thus exerts neuroblastoma growth control similar to galectin-1 despite their structural differences. In addition to p53-linked proapoptotic activity intracellularly, galectin-7, acting as a lectin on the cell surface, appears to be capable of reducing cancer cell proliferation in susceptible systems.
引用
收藏
页码:6277 / 6288
页数:12
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