| First Author | Hébert E | Year | 1997 |
| Journal | Biol Cell | Volume | 89 |
| Issue | 7 | Pages | 467-73 |
| PubMed ID | 9561725 | Mgi Jnum | J:49450 |
| Mgi Id | MGI:1277495 | Doi | 10.1016/s0248-4900(97)89317-3 |
| Citation | Hebert E, et al. (1997) Lack of modulation of the galectin-3 and asialoglycoprotein receptor transcription in hepatocarcinoma of transgenic mice. Biol Cell 89(7):467-73 |
| abstractText | Galectin-3 and asialoglycoprotein receptor are lectins belonging to the classes of soluble lectins and of membrane C type lectins respectively. Conflicting results have been reported concerning their transcription level in the time course development of tumours. In the present study we investigated the abnormalities and the transcription levels of galectin-3 and asialoglycoprotein receptor genes in liver-targeted SV40 large T transgenic mice related to normal mice. In the strain expressing 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 galectin-3 gene is weakly transcribed and its level is identical and constant in normal and transgenic mice, suggesting a lack of involvement in the development of large T-induced hepatocarcinoma. The asialoglycoprotein receptor gene is actively transcribed and its level remains high all along the development of the tumour; therefore, in such an hepatocarcinoma the asialoglycoprotein receptor could be used to take up drugs, genes or oligonucleotides associated with glycosylated carriers bearing galactose residues in a terminal non-reducing position. |
