DocumentCode
2190473
Title
Inhibition of ppGalNacT2 at Protein Level Contributes to Vanadium Induced HL-60 Cell Apoptosis
Author
Gaoyuan Guoyi ; Xulan Wushiliang
Author_Institution
Dept. of Biochem. & Mol. Biol., Soochow Univ., Suzhou, China
fYear
2009
fDate
17-19 Oct. 2009
Firstpage
1
Lastpage
7
Abstract
In this study we docked one compound substances of vanadium in the body, V03 (molecular formula 013V4, partial vanadate tetramer) and ppGalNAcT2, which shows that V03 may inhibit the activity of the enzyme by stopping conformational changes of a key loop of ppGalNAcT2. Besides, through experiments we discovered that at mRNA level, ppGalNAc-T2 changed with the variation of HL-60 cell growth induced by vanadium. Then we respectively transfected HL-60 cell with ppGalNAc-T2 RNA Interferential Carrier (pSilenCircle, T2-Si) and Vacuity Carrier (T2-Scr). We found the expression of ppGalNacT-2 not only inhibited low dose vanadium induced cell proliferation, but also influenced cell sticking. Taken together, our results suggested that inhibited the expression of ppGalNacT2 together with vanadium have synergic anti-tumor effects, which providing a new mechanism of vanadium anti-tumor effect and indicating that inhibitors of ppGalNacT-2 may enhance the therapeutic efficiency of vanadium for leucemia.
Keywords
enzymes; molecular biophysics; tumours; HL-60 cell apoptosis; antitumor effect; cell growth; conformational change; enzyme; leucemia; mRNA level; ppGalNacT2 inhibition; protein level; Biochemistry; Cancer; Cells (biology); Chemical elements; Humans; Neoplasms; Proteins; RNA; Testing; Tumors;
fLanguage
English
Publisher
ieee
Conference_Titel
Biomedical Engineering and Informatics, 2009. BMEI '09. 2nd International Conference on
Conference_Location
Tianjin
Print_ISBN
978-1-4244-4132-7
Electronic_ISBN
978-1-4244-4134-1
Type
conf
DOI
10.1109/BMEI.2009.5305372
Filename
5305372
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