CAJ | 학술논문

目的：观察转化生长因子β1（TGF-β1）对人胃癌SGC7901细胞增殖和凋亡的影响，探讨其可能的作用机制。方法使用不同浓度的TGF-β1（0.5、1、2、5、ng·mL-1）干预人胃癌细胞SGC7901不同时间（6、12、24、48、72h），通过MTT法检测细胞生长抑制率，流式细胞仪检测细胞凋亡情况，RT-PCR法检测细胞内Smad3、Smad7 mRNA的表达水平。结果（1）在0.5～10 ng·mL-1的浓度范围内，TGF-β1以剂量依赖性方式抑制胃癌SGC7901细胞增殖，并表现出明显的量效关系（r=0.908， P<0.01）；且随着作用时间的延长，TGF-β1对胃癌SGC7901细胞的抑制率逐渐升高，呈时间依赖性。5 ng·mL-1及10 ng·mL-1 TGF-β1作用于胃癌SGC7901细胞72 h后，生长抑制率分别为（61.12±0.98）％、（63.67±0.18）％（与无TGF-β1处理组相比， P<0.01），抑制作用相当。（2）5 ng·mL-1 TGF-β1作用于人胃癌SGC7901细胞不同时间（0、6、12、24、48、72 h）后，细胞凋亡率没有明显改变（P>0.05），分别为1.32%、2.61%、3.15%、3.31%、3.76%、3.82%；10 ng·mL-1 TGF-β1作用于人胃癌SGC7901细胞不同时间（0、6、12、24、48、72 h）后，细胞凋亡率没有明显改变（P>0.05），分别为1.88%、2.57%、1.57%、1.67%、2.04%、4.58%。（3）0.5～10 ng·mL-1 TGF-β1作用于人胃癌SGC7901细胞时，TGF-β1以剂量依赖性方式增加胃癌SGC7901细胞Smad3、Smad7的mRNA表达（与无TGF-β1处理组相比，P<0.01）。结论 TGF-β1可以浓度和剂量依赖性方式抑制胃癌SGC7901细胞的增殖，这可能与其增加smad3和smad7的mRNA表达有关，但TGF-β1并不能促进胃癌SGC7901细胞的凋亡。
목적：관찰전화생장인자β1（TGF-β1）대인위암SGC7901세포증식화조망적영향，탐토기가능적작용궤제。방법사용불동농도적TGF-β1（0.5、1、2、5、ng·mL-1）간예인위암세포SGC7901불동시간（6、12、24、48、72h），통과MTT법검측세포생장억제솔，류식세포의검측세포조망정황，RT-PCR법검측세포내Smad3、Smad7 mRNA적표체수평。결과（1）재0.5～10 ng·mL-1적농도범위내，TGF-β1이제량의뢰성방식억제위암SGC7901세포증식，병표현출명현적량효관계（r=0.908， P<0.01）；차수착작용시간적연장，TGF-β1대위암SGC7901세포적억제솔축점승고，정시간의뢰성。5 ng·mL-1급10 ng·mL-1 TGF-β1작용우위암SGC7901세포72 h후，생장억제솔분별위（61.12±0.98）％、（63.67±0.18）％（여무TGF-β1처리조상비， P<0.01），억제작용상당。（2）5 ng·mL-1 TGF-β1작용우인위암SGC7901세포불동시간（0、6、12、24、48、72 h）후，세포조망솔몰유명현개변（P>0.05），분별위1.32%、2.61%、3.15%、3.31%、3.76%、3.82%；10 ng·mL-1 TGF-β1작용우인위암SGC7901세포불동시간（0、6、12、24、48、72 h）후，세포조망솔몰유명현개변（P>0.05），분별위1.88%、2.57%、1.57%、1.67%、2.04%、4.58%。（3）0.5～10 ng·mL-1 TGF-β1작용우인위암SGC7901세포시，TGF-β1이제량의뢰성방식증가위암SGC7901세포Smad3、Smad7적mRNA표체（여무TGF-β1처리조상비，P<0.01）。결론 TGF-β1가이농도화제량의뢰성방식억제위암SGC7901세포적증식，저가능여기증가smad3화smad7적mRNA표체유관，단TGF-β1병불능촉진위암SGC7901세포적조망。
Objective To investigate the impact of transforming growth factor beta 1 (TGF-β1) on proliferation and apoptosis of human gastric cancer cell SGC7901, and discuss its possible mechanism. Methods After the human gastric cancer cells SGC7901 were intervened by different concentrations of TGF-β1 (0.5, 1, 2, 5, 10 ng·mL-1) for different period of time (6, 12, 24, 48, 72 h), the cell growth inhibition rate and cell apoptosis were determined respectively by MTT method and flow cytometry. The mRNA expression levels of Smad3 and Smad7 were detected by RT-PCR. Results (1) Within the concentration range 0.5~10 ng·mL-1, TGF-β1 inhibited the proliferation of SGC7901 cells in a dose-dependent manner, and showed an obvious dose-effect relationship (r=0.908, P<0.01). Along with the extension of treating time, the TGF-β1 inhibition ratio to SGC7901 cells also gradually increased, showing concentration dependence and time dependence. Af-ter the SGC-7901 cells had been treated for 72 h by 5 ng·mL-1 or 10 ng·mL-1 of TGF-β1, the growth inhibition ratio was respectively (61.12 ±0.98)%and (63.67±0.18)%in comparison with none TGF-β1 treatment group(P<0.01);the inhibition effect was relatively equal. (2)After the SGC7901 cells had been treated by 5 ng·mL-1 of TGF-β1 for different period of time (0, 6, 12, 24, 48, 72 h), the cell apoptosis rate was respectively 1.32%, 2.61%, 3.15%, 3.31%, 3.76%and 3.82%, having no significant differences (P>0.05). Even after treatment of 10 ng·mL-1 TGF-β1 for different period of time (0, 6, 12, 24, 48, 72 h), the cell apoptosis rate was not significantly changed (P>0.05), and was respectively 1.88%、2.57%、1.57%、1.67%、2.04%and 4.58%. (3) The expression of Smad3 and Smad7 in SGC7901 cells increased in a dose-dependent manner after treatment of TGF-β1 within a concentration range 0.5~10 ng·mL-1 (compared with no TGF-β1 treatment group, P<0.01). Conclusions TGF-β1 could inhibit the prolif-eration of SGC7901 gastric cancer cells in a concentration and dose-dependent way. It may be related to its up-regulation on the mRNA expression of smad3 and smad7. But the TGF-β1 did not promote the apoptosis of SGC7901 gastric cancer cells.