| Journal of biosciences | |
| GalNAc-T14 may be involved in regulating the apoptotic action of IGFBP-3 | |
| Yaojun Shan4  Wenqian Song4  Minji Zou1  Donggang Xu41  Min Wang1  Chen Wu4  Xinxia Liu3  Jiali Wang2  | |
| [1] Institute of Basic Medical Sciences, Beijing 100850, P R China$$;College of Pharmaceutical Sciences, Hebei University, Baoding, Hebei, 071002, P R China$$;Health Sciences Centre, Hebei University, Baoding, Hebei, 071002, P R China$$;College of Life Sciences, Hebei University, Baoding, Hebei, 071002, P R China$$ | |
| 关键词: Apoptosis; GalNAc-T14; IGFBP-3; RNAi; | |
| DOI : | |
| 来源: Indian Academy of Sciences | |
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【 摘 要 】
Insulin-like growth factor binding protein-3 (IGFBP-3) is known to induce apoptosis in an insulin-like growth factor (IGF)-dependent and IGF-independent manner, but the mechanism underlying the IGF-independent effects remains unclear. Polypeptide ð‘-acetylgalactosaminyltransferase 14 (GalNAc-T14) is a novel IGFBP-3 binding partner. In this paper, small interference RNA (siRNA) targeting GalNAc-T14 was used to examine whether GalNAc-T14 affects the apoptotic action of IGFBP-3. Using semi-quantitative reverse-transcriptase polymerase chain reaction (RT-PCR) and western blot analysis, we determined that GalNAc-T14 expression was downregulated by the siRNA directed against GalNAc-T14. Apoptosis analysis of IGFBP-3-overexpressing cells treated with siRNA against GalNAc-T14 was performed to determine if GalNAc-T14 was specifically involved in IGFBP-3 signalling. The results, as determined by flow cytometric analysis and caspase-3 assay, showed that the extent of apoptosis induced by IGFBP-3 increased with RNA interference (RNAi) knockdown of GalNAc-T14. Our data suggest that GalNAc-T14 influences the apoptotic action of IGFBP-3 and might mediate the signalling pathway of IGFBP-3. Experiments to determine the role of GalNAc-T14 in the regulation of apoptosis induced by IGFBP-3 are under way.
【 授权许可】
Unknown
【 预 览 】
| Files | Size | Format | View |
|---|---|---|---|
| RO201912040494835ZK.pdf | 679KB |
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