| First Author | Wei Y | Year | 2010 |
| Journal | Biochem Biophys Res Commun | Volume | 396 |
| Issue | 3 | Pages | 602-7 |
| PubMed ID | 20417617 | Mgi Jnum | J:162515 |
| Mgi Id | MGI:4819078 | Doi | 10.1016/j.bbrc.2010.04.110 |
| Citation | Wei Y, et al. (2010) Beta1,4-galactosyltransferase V regulates self-renewal of glioma-initiating cell. Biochem Biophys Res Commun 396(3):602-7 |
| abstractText | Glioma results from unregulated expansion of a self-renewing glioma-initiating cell population. The regulatory pathways which are essential for sustaining the self-renewal of glioma-initiating cells remain largely unknown. Cell surface N-linked oligosaccharides play functional roles in determining cell fate and are associated with glioma malignancy. Previously, we have reported that beta1,4-galactosyltransferase V (beta1,4GalT V) effectively galactosylates the GlcNAcbeta1-->6Man arm of the highly branched N-glycans and positively regulates glioma cell growth. Here, we show that decreasing the expression of beta1,4GalT V by RNA interference in glioma cells attenuated the formation of polylactosamine and inhibited the ability of tumor formation in vivo. Down-regulation of beta1,4GalT V depleted CD133-positive cells in glioma xenograft, and inhibited the self-renewal capacity and the tumorigenic potential of glioma-initiating cells. These data reveal a critical role of beta1,4GalT V in the self-renewal and tumorigenicity of glioma-initiating cells, and indicate that manipulating beta1,4GalT V expression may have therapeutic potential for the treatment of malignant glioma. |
