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Inhibition of N-acetylglucosaminyltransferase V enhances sensitivity of radiotherapy in human prostate cancer.

Abstract
The purpose of this study was to investigate the relationship between N-acetylglucosaminyltransferase V (GnT-V) and radiation sensitivity of prostate cancer (PCa) cells both in vitro and in vivo. Firstly, the GnT-V expression was studied in 84 cases of PCa tissues, in which higher level of GnT-V was detected more frequently in the advanced tumors. Secondly, the GnT-V stably suppressed cell lines PCa/1079 (Lncap/1079 and PC3/1079) were constructed from PCa cell lines (Lncap and PC3) in vitro. Attenuation of GnT-V inhibited cell proliferation, migration and increased apoptosis, which resulted in enhanced radiation sensitivity of PCa cells. The underlying mechanism may be relevant to the increasing ratio of Bax/Bcl-2, the blocking transcription of NF-κB and the reduction of cell cycle G2-M arrest. Finally, in in vivo study, compared with control groups, the irradiated PCa xenograft nude mice of PCa/1079 indicated to reduce tumor-growth rate and enhance survival time. Summary, our studies showed that inhibition of GnT-V probably improved PCa cells' radiation sensitivity.
AuthorsHuiyi Huang, Wenxia Chen, Qiulian Liu, Ting Wei, Weiliang Zhu, Hui Meng, Linlang Guo, Jian Zhang
JournalBiochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 451 Issue 3 Pg. 345-51 (Aug 29 2014) ISSN: 1090-2104 [Electronic] United States
PMID25117443 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2014 Elsevier Inc. All rights reserved.
Chemical References
  • N-Acetylglucosaminyltransferases
  • alpha-1,6-mannosylglycoprotein beta 1,6-N-acetylglucosaminyltransferase
Topics
  • Animals
  • Apoptosis (radiation effects)
  • Cell Line, Tumor
  • Cell Movement (drug effects)
  • Cell Proliferation (drug effects)
  • Down-Regulation
  • Humans
  • Male
  • Mice
  • Mice, Nude
  • N-Acetylglucosaminyltransferases (antagonists & inhibitors, biosynthesis)
  • Prostatic Neoplasms (radiotherapy)
  • Radiation Tolerance (drug effects, genetics)

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