AIM:To investigate the role of TR3 in induction of apoptosisin gastric cancer cells.METHODS:Human gastric cancer cell line,MGC80-3,wasused.Expression of TR3 mRNA and its protein was detectedby Northern blot and Western blot.Localization of TR3protein was showed by immunofluorescence analysis underlaser-scanning confocal microscope.Apoptotic morphologywas observed by DAPI fluorescence staining,and apoptoticindex was counted among 1000 cells randomly.Stabletransfection assay was carried out by Lipofectamine.RESULTS:Treatment of MGC80-3 cells with TPA and VP-16resulted in apoptosis,accompanied by the repression ofBcl-2 protein in a time-dependent manner.At the sametime,TPA and VP-16 also up-regulated expression level ofTR3 mRNA in MGC80-3 cells that expressed TR3 mRNA.When antisense-TR3 expression vector was transfected intothe cells,expression of TR3 protein was repressed.In thiscase,TPA and VP-16 did not induce apoptosis.In addition,TPA and VP-16-induced apoptosis involved in translocationof TR3.In MGC80-3 cells,TR3 localized concentrative innucleus,after treatment of cells with TPA and VP-16,TR3translocated from nucleus to cytosol obviously.However,when this nuclear translocation was blocked by LMB,apoptosis was not occurred in MGC80-3 cells even in thepresence of TPA and VP-16.CONCLUSION:Induction of apoptosis by TPA and VP-16 isthrough induction of TR3 expression and translocation of TR3from nucleus to cytosol,which may he a novel signalpathway for TR3,and represent the new biological function ofTR3 to exert its effect on apoptosis in gastric cancer cells. AIM: To investigate the role of TR3 in induction of apoptosis in gastric cancer cells. METHODS: Human gastric cancer cell line, MGC80-3, was used. Expression of TR3 mRNA and its protein was detected by Northern blot and Western blot. Localization of TR3 protein showed was by immunofluorescence analysis underlaser-scanning confocal microscope. Apoptotic morphology was observed by DAPI fluorescence staining, and apoptoticindex was counted among 1000 cells randomly. Stabletransfection assay was carried out by Lipofectamine. RESULTS: Treatment of MGC80-3 cells with TPA and VP-16 resulted in apoptosis , accompanied by the repression of Bcl-2 protein in a time-dependent manner. At the same time, TPA and VP-16 also up-regulated expression level of TR3 mRNA in MGC80-3 cells that expressed TR3 mRNA.When antisense-TR3 expression vector was transfected intothe cells, expression of TR3 protein was repressed.In this case, TPA and VP-16 did not induce apoptosis. In addition, TPA and VP-16-induced apoptosis involved in translocat ionof TR3.In MGC80-3 cells, TR3 localized concentrative innucleus, after treatment of cells with TPA and VP-16, TR3 transnslocated from nucleus to cytosol obviously. Host, when this nuclear translocation was blocked by LMB, apoptosis was not caused in MGC80- 3 cells even in the presence of TPA and VP-16.CONCLUSION: Induction of apoptosis by TPA and VP-16 isthrough induction of TR3 expression and translocation of TR3 from nucleus to cytosol, which may he a novel signal pathway for TR3, and the new biological function ofTR3 to exert its effect on apoptosis in gastric cancer cells.