LACK OF MODULATION OF THE GALECTIN-3 AND ASIALOGLYCOPROTEIN RECEPTOR TRANSCRIPTION IN HEPATOCARCINOMA OF TRANSGENIC MICE

Citation
E. Hebert et M. Monsigny, LACK OF MODULATION OF THE GALECTIN-3 AND ASIALOGLYCOPROTEIN RECEPTOR TRANSCRIPTION IN HEPATOCARCINOMA OF TRANSGENIC MICE, Biology of the cell, 89(7), 1997, pp. 467-473
Citations number
49
Categorie Soggetti
Cell Biology
Journal title
ISSN journal
02484900
Volume
89
Issue
7
Year of publication
1997
Pages
467 - 473
Database
ISI
SICI code
0248-4900(1997)89:7<467:LOMOTG>2.0.ZU;2-Q
Abstract
Galectin-3 and asialoglycoprotein receptor are lectins belonging to th e classes of soluble lectins and of membrane C type lectins respective ly. Conflicting results have been reported concerning their transcript ion level in the time course development of tumours. In the present st udy we investigated the abnormalities and the transcription levels of galectin-3 and asialoglycoprotein receptor genes in liver-targeted SV4 0 large T transgenic mice related to normal mice. in the strain expres sing the highest level of large T, 100% of the male mice reproducibly developed an hepatocarcinoma. We provide evidence that the galectin-3 and asialoglycoprotein receptor genes are stable in such mice. The gal ectin-3 gene is weakly transcribed and its level is identical and cons tant in normal and transgenic mice, suggesting a lack of involvement i n the development of large T-induced hepatocarcinoma. The asialoglycop rotein receptor gene is actively transcribed and its level remains hig h all along the development of the tumour; therefore, in such an hepat ocarcinoma the asialoglycoprotein receptor could be used to take up dr ugs, genes or oligonucleotides associated with glycosylated carriers b earing galactose residues in a terminal non-reducing position. ((C) El sevier, Paris).