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

Jürgen Kopitz; Sabine André; Carolina Von Reitzenstein; Kees Versluis; Herbert Kaltner; Roland J. Pieters; Kojiro Wasano; Ichiro Kuwabara; Fu-Tong Liu; Michael Cantz; Albert J R Heck; Hans Joachim Gabius

doi:10.1038/sj.onc.1206631

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

Jürgen Kopitz, Sabine André, Carolina Von Reitzenstein, Kees Versluis, Herbert Kaltner, Roland J. Pieters, Kojiro Wasano, Ichiro Kuwabara, Fu-Tong Liu, Michael Cantz, Albert J R Heck, Hans Joachim Gabius

Dermatology

Research output: Contribution to journal › Article › peer-review

133 Scopus citations

Abstract

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.

Original language	English (US)
Pages (from-to)	6277-6288
Number of pages	12
Journal	Oncogene
Volume	22
Issue number	40
DOIs	https://doi.org/10.1038/sj.onc.1206631
State	Published - Sep 18 2003

Keywords

Apoptosis
Cell growth
Galectin
Ganglioside
Mass spectrometry
Neuroblastoma

ASJC Scopus subject areas

Molecular Biology
Cancer Research
Genetics

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Homodimeric galectin-7 (p53-induced gene 1) is a negative growth regulator for human neuroblastoma cells. / Kopitz, Jürgen; André, Sabine; Von Reitzenstein, Carolina; Versluis, Kees; Kaltner, Herbert; Pieters, Roland J.; Wasano, Kojiro; Kuwabara, Ichiro; Liu, Fu-Tong; Cantz, Michael; Heck, Albert J R; Gabius, Hans Joachim.

In: Oncogene, Vol. 22, No. 40, 18.09.2003, p. 6277-6288.

Research output: Contribution to journal › Article › peer-review

Kopitz, Jürgen ; André, Sabine ; Von Reitzenstein, Carolina ; Versluis, Kees ; Kaltner, Herbert ; Pieters, Roland J. ; Wasano, Kojiro ; Kuwabara, Ichiro ; Liu, Fu-Tong ; Cantz, Michael ; Heck, Albert J R ; Gabius, Hans Joachim. / Homodimeric galectin-7 (p53-induced gene 1) is a negative growth regulator for human neuroblastoma cells. In: Oncogene. 2003 ; Vol. 22, No. 40. pp. 6277-6288.

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abstract = "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.",

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

Abstract

Keywords

ASJC Scopus subject areas

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