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Objective and methods:In this study,it was investigated for the effects of human selenoprotein SelK on the adhesion and migration ability of human gastric cancer BGC-823 cells using matrigel adhesion and transwell migration assays,respectively.Results:The matrigel adhesion ability of BGC-823 cells that overexpressed SelK declined extremely significantly（P<0.01）,compared with that of the cells not expressing the protein.The migration ability of BGC-823 cells that overexpressed SelK also declined extremely significantly（P<0.01）.On the other hand,the matrigel adhesion ability and the migration ability of the cells that overexpressed C-terminally truncated SelK not declined significantly.And the matrigel adhesion ability and the migration ability of human embryonic kidney HEK-293 cells that overexpressed SelK did not express significant change（P>0.05） with the cells that overexpressed the C-terminally truncated protein.In addition to the effect on matrigel adhesion and migration,the overexpression of SelK also caused a loss in cell viability（as measured by 3-（4,5-dimethyl-2-thiazolyl）-2,5-diphenyl-2H tetrazolium bromide（MTT） colorimetric assay） and induced apoptosis as shown by confocal microscopy and flow cytometry.The cytosolic free Ca2+ level of these cells was significantly increased as detected by flow cytometry.But the overexpression of SelK in HEK-293 cells did not cause a significant loss in cell viability or induce apoptosis.Only the elevation of cytosolic free Ca2+ level in these cells was significant.Conclusions:Taken together,the results suggested that SelK could inhibit human cancer cells’ matrigel adhesion and migration,the loss in cell viability and induction of apoptosis,resulting from the release of intracellular Ca from the endoplasmic reticulum might be one of the mechanisms whereby the protein exerted its impact.Furthermore,only the full-length protein was capable of producing such impact since the C-terminally truncated form appeared to have no impact.The embryonic cells were not influenced by the elevation of free Ca2+ level in cytosol probably due to their much more tolerance to the variation.