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Journal of Cancer Prevention

Original Article

Cancer prevention research 2010; 15(4): 313-319

Published online December 30, 2010

© Korean Society of Cancer Prevention

Apoptotic Effects of Selenium via AMPK-VASP Signal Pathway in B16F10 Melanoma Cells

Song Yi Park1, Sol Hwa Lee1, Ock Jin Park2 and Young Min Kim1

Abstract

A vasodilatator-stimulierte phosphoprotein (VASP), Ena/VASP family, is connected to actin. It is associated with the signal pathway involving the proliferation and migration of cells, and VASP regulates cells-cells contacts. VASP in the blood acts as cAMP-and cGMP-dependent protein kinase. According to the positions of amino acid at Ser-157, Ser-239 and Thr-278, it is regulated by AMP-activated protein kinase (AMPK) that acts as Ser-Thr kinase. Recently the VASP is known to the new substrate of AMPK. The AMPK plays a role of the energy sensor. If AMPK is activated in cancer cells, apoptosis is induced in them. However, activation of mTOR is known to be promoted cancer growth. In addition, Akt, which is a kind of Ser-Thr kinase, is responsible for proliferation, differentiation, and growth of cells, and it inhibits apoptosis in cancer cells and is known to engage in angiogenesis and metastasis. In this study, when selenium is treated in B16F10 cancer cells, we suggest that the growth of B16F10 cells is inhibited. We determined with MTT assay, Fluorescence-Activated Cell Sorting (FACS), and Western blotting. Finally, it is observed whether these inhibitory effects is due to induction of apoptosis, and we have tried to evaluate the anti-tumor effect of selenium, through VASP, AMPK, mTOR and Akt signal pathway. (Cancer Prev Res 15, 313-319, 2010)

Keywords: Selenium, Apoptosis, B16F10 melanoma cells, AMPK, VASP

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