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Inhibition of ppGalNacT2 at Protein Level Contributes to Vanadium Induced HL-60 Cell Apoptosis

In this study we docked one compound substances of vanadium in the body, VO3 (molecular formula O13V4, partial vanadate tetramer) and ppGalNAcT2, which shows that VO3 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 ppGalNacT- 2 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-polypeptide N-acetylgalactosaminyl-transferase-2 (ppGalNAc-T2); vanadium; leukemic cell HL-60; molecular dynamics