Next Article in Journal
Salvianolic Acid A, as a Novel ETA Receptor Antagonist, Shows Inhibitory Effects on Tumor in Vitro
Next Article in Special Issue
Phylogenetic-Derived Insights into the Evolution of Sialylation in Eukaryotes: Comprehensive Analysis of Vertebrate β-Galactoside α2,3/6-Sialyltransferases (ST3Gal and ST6Gal)
Previous Article in Journal
Association of Serum Uric Acid Concentration with Diabetic Retinopathy and Albuminuria in Taiwanese Patients with Type 2 Diabetes Mellitus
Previous Article in Special Issue
Predominant Expression of Hybrid N-Glycans Has Distinct Cellular Roles Relative to Complex and Oligomannose N-Glycans
Article Menu
Issue 8 (August) cover image

Export Article

Open AccessArticle
Int. J. Mol. Sci. 2016, 17(8), 1246;

Upregulation of Human ST8Sia VI (α2,8-Sialyltransferase) Gene Expression by Physcion in SK-N-BE(2)-C Human Neuroblastoma Cells

Department of Medicinal Biotechnology, College of Health Sciences, Dong-A university, Busan 49315, Korea
Department of Horticultural Bioscience, Pusan National University, Miryang 50463, Korea
Research Center for Anti-Aging Technology Development, Pusan National University, Busan 46241, Korea
Molecular and Cellular Glycobiology Unit, Department of Biological Sciences, SungKyunKwan University, Kyunggi-Do 16419, Korea
These authors contributed equally to this work.
Authors to whom correspondence should be addressed.
Academic Editor: Li Yang
Received: 3 June 2016 / Revised: 28 June 2016 / Accepted: 25 July 2016 / Published: 2 August 2016
(This article belongs to the Special Issue Glycan–Receptor Interaction)
Full-Text   |   PDF [4361 KB, uploaded 2 August 2016]   |  


In this research, we firstly demonstrated that physcion, an anthraquinone derivative, specifically increased the expression of the human α2,8-sialyltransferase (hST8Sia VI) gene in SK-N-BE(2)-C human neuroblastoma cells. To establish the mechanism responsible for the up-regulation of hST8Sia VI gene expression in physcion-treated SK-N-BE(2)-C cells, the putative promoter region of the hST8Sia VI gene was functionally characterized. Promoter analysis with serially truncated fragments of the 5′-flanking region showed that the region between −320 and −240 is crucial for physcion-induced transcription of hST8Sia VI in SK-N-BE(2)-C cells. Putative binding sites for transcription factors Pax-5 and NF-Y are located at this region. The Pax-5 binding site at −262 to −256 was essential for the expression of the hST8Sia VI gene by physcion in SK-N-BE(2)-C cells. Moreover, the transcription of hST8Sia VI induced by physcion in SK-N-BE(2)-C cells was inhibited by extracellular signal-regulated protein kinase (ERK) inhibitor U0126 and p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580, but not c-Jun N-terminal kinase (JNK) inhibitor SP600125. These results suggest that physcion upregulates hST8Sia VI gene expression via ERK and p38 MAPK pathways in SK-N-BE(2)-C cells. View Full-Text
Keywords: physcion; hST8Sia VI; SK-N-BE(2)-C; transcription factor Pax-5; signal pathway physcion; hST8Sia VI; SK-N-BE(2)-C; transcription factor Pax-5; signal pathway

Graphical abstract

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Supplementary material


Share & Cite This Article

MDPI and ACS Style

Yoon, H.-K.; An, H.-K.; Ko, M.J.; Kim, K.-S.; Mun, S.-W.; Kim, D.-H.; Kim, C.M.; Kim, C.-H.; Choi, Y.W.; Lee, Y.-C. Upregulation of Human ST8Sia VI (α2,8-Sialyltransferase) Gene Expression by Physcion in SK-N-BE(2)-C Human Neuroblastoma Cells. Int. J. Mol. Sci. 2016, 17, 1246.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top