AIM:To study the moleucle action mechunisms of NM-3 onthe growth of human gastric cancer SGC-7901 cells in vivoor in vitro.METHODS:SGC-7901 from human non-differentiatedgastric cancer cell line was cultured with NM-3 at 100 mg/mlfor 24 h.We observed its inhibitory rate and the density ofmicro-vascular growth in grafted mice with human gastriccancer SGC-7901.The apoptosis of human gastric cancerSGC-7901 was revealed in NM-3 treatment group by usingterminal deoxynucleotidyl transferase-mediated deoxy-uridine triphosphate-fluorescene nick end labeling (TUNEL)method and flow cytometry analysis.RESULTS:The growth of SGC-7901 cells was markedlyinhibited compared with control growp,which was smallerthan that in normal saline control group (4.17 g±0.22 g vs9.45 g±1.38 g,P<0.01).The level of apoptosis of humangastric cell line SGC-7901 was obviously increased in NM-3treatment group at 1 mg.L~(-1) for 24 h.NM-3 inducing apoptoticindex in NM-3 plus carboplatin group was 3.5 times thatof carboplatin control group (TUNEL:27.98±6.12% vs12.94±2.12%,FACScan:26.86±5.69% vs 11.86±1.09%,P<0.01).Western blot analysis showed that the apoptoticindex of human gastric cancer was elevated for 12,24 and36 h with an evident time-effect relationship in groups at100 mg.L~(-1).NM-3 enhanced the inhibitive effects andsensitivity of chemotherapy for human gastric cancer innude mice.These results suggested that NM-3 played akey inhibitive role in the growth of grafted human gastriccancer in nude mice.CONCLUSION:NM-3 can inhibit the growth of humangastric cancer cell line SGC-7901,and enhance thesensitivity of carboplatin on SGC-7901 and induced itsapoptosis. AIM: To study the moleuclei action mesenisms of NM-3 on the growth of human gastric cancer SGC-7901 cells in vivoor in vitro. METHODS: SGC-7901 from human non-differentiated gastric cancer cell line was cultured with NM-3 at 100 mg / ml for 24 h. We observed its inhibitory rate and the density of micro-vascular growth in grafted mice with human gastric cancer SGC-7901. The apoptosis of human gastric cancer SGC-7901 was revealed in NM-3 treatment group by using terminator deoxynucleotidyl transferase-mediated deoxy- uridine triphosphate-fluorescene nick end labeling (TUNEL) method and flow cytometry analysis. RESULTS: The growth of SGC-7901 cells was markedly inhibited compared with control growp, which was smallerthan that in normal saline control group (4.17 g ± 0.22 g vs 9.45 g ± 1.38 g, P <0.01). The level of apoptosis of humangastric cell line SGC-7901 was significantly increased in NM-3 treatment group at 1 mg.L -1 for 24 h.NM-3 inducing apoptoticindex in NM -3 plus carboplatin group was 3.5 times thatof carbopl atin control group (TUNEL: 27.98 ± 6.12% vs 12.94 ± 2.12%, FACScan: 26.86 ± 5.69% vs 11.86 ± 1.09%, P <0.01). Western blot analysis showed that the apoptotic index of human gastric cancer was elevated for 12, 24 and 36 h with an evident time-effect relationship in groups at 100 mg. L -1. NM-3 enhanced the inhibitive effects and sensitivity of chemotherapy for human gastric cancer innude mice. These results suggested that NM-3 played a key inhibitive role in the growth of grafted human gastric cancer in nude mice. CONCLUSION: NM-3 can inhibit the growth of humangastric cancer cell line SGC-7901, and enhance these sensitivity of carboplatin on SGC-7901 and induced its apoptosis.