CAJ | 학술논문

目的：探讨 Gal -1蛋白促胃癌细胞侵袭转移的可能机制。方法采用0、1和5μg/ mL 的 Gal -1蛋白体外刺激胃癌细胞，利用肿瘤细胞侵袭模型分析 Gal -1蛋白对胃癌细胞侵袭迁移能力的影响；利用 WB 实验和明胶酶谱法，分别检测 Gal -1蛋白刺激前后胃癌细胞中 MMP -9的表达及活性变化，分析 Gal -1促胃癌转移的可能分子机制。结果细胞迁移实验显示，胃癌细胞 BGC -823经1和5μg/ mL 的 Gal -1蛋白刺激后穿膜细胞数分别为（117±8.19）和（167±7.55）个，明显高于0μg/ mL 组的（67±4.58）个（P ＜0.05）；胃癌7901细胞经1和5μg/ mL 的 Gal -1蛋白刺激后穿膜细胞数分别为（151±5.13）和（190.3±6.8）个，高于0μg/ mL组的（87±6.56）个（P ＜0.05）。细胞侵袭实验显示，BGC -823经1和5μg/ mL 的 Gal -1蛋白刺激后穿膜细胞数分别为（51±3.6）和（76.7±9.07）个，明显高于0μg/ mL 组的（22.7±4.16）个（ P ＜0.05）；胃癌7901细胞经1和5μg/ mL 的 Gal -1蛋白刺激后穿膜细胞数分别为（74.0±7.21）和（105.3±11.37）个，高于0μg/ mL组的（42.3±6.66）个（P ＜0.05）。WB 实验显示，经 Gal -1蛋白刺激后，胃癌细胞中 MMP -9的表达增高。明胶酶谱实验显示，Gal -1蛋白刺激后，MMP -9酶活性增强。结论 Gal -1蛋白能促进胃癌细胞的侵袭迁移能力，可能与其能增强胃癌细胞中的 MMP -9表达和活性有关。
목적：탐토 Gal -1단백촉위암세포침습전이적가능궤제。방법채용0、1화5μg/ mL 적 Gal -1단백체외자격위암세포，이용종류세포침습모형분석 Gal -1단백대위암세포침습천이능력적영향；이용 WB 실험화명효매보법，분별검측 Gal -1단백자격전후위암세포중 MMP -9적표체급활성변화，분석 Gal -1촉위암전이적가능분자궤제。결과세포천이실험현시，위암세포 BGC -823경1화5μg/ mL 적 Gal -1단백자격후천막세포수분별위（117±8.19）화（167±7.55）개，명현고우0μg/ mL 조적（67±4.58）개（P ＜0.05）；위암7901세포경1화5μg/ mL 적 Gal -1단백자격후천막세포수분별위（151±5.13）화（190.3±6.8）개，고우0μg/ mL조적（87±6.56）개（P ＜0.05）。세포침습실험현시，BGC -823경1화5μg/ mL 적 Gal -1단백자격후천막세포수분별위（51±3.6）화（76.7±9.07）개，명현고우0μg/ mL 조적（22.7±4.16）개（ P ＜0.05）；위암7901세포경1화5μg/ mL 적 Gal -1단백자격후천막세포수분별위（74.0±7.21）화（105.3±11.37）개，고우0μg/ mL조적（42.3±6.66）개（P ＜0.05）。WB 실험현시，경 Gal -1단백자격후，위암세포중 MMP -9적표체증고。명효매보실험현시，Gal -1단백자격후，MMP -9매활성증강。결론 Gal -1단백능촉진위암세포적침습천이능력，가능여기능증강위암세포중적 MMP -9표체화활성유관。
Objective To explore the possible mechanisms of Galectin - 1(Gal - 1)protein in promoting the invasion and migration of gastric cancer cells. Methods After treated with different concentrations(0,1,5 μg/ mL)of Gal - 1 protein, the Trans - well model was used to analyze the invasion and migration ability of gastric cancer. WB and gelatin zymography method were used to detect the MMP - 9 expression and active form change in gastric cancer cells after Gal - 1 stimulate, in order to explore the possible molecular mechanisms of Gal - 1 protein in promoting the invasion and migration of gastric cancer cells. Results In cell migration assay,the number of gastric cancer cells BGC - 823 treated with 1and 5 μg/ mL Gal - 1 stimulate were 117 ± 8. 19 and 167 ± 7. 55,higher than that treated with 0 μg/ mL(P < 0. 05). The number of gastric cancer cells 7 901 treated with 1and 5 μg/ mL Gal - 1 stimulate were 151 ± 5. 13 and 190. 3 ± 6. 8,higher than that treated with 0 μg/ mL(P < 0. 05). In cell invasion assay,the number of gastric cancer cells BGC - 823 treated with 1and 5μg/ mL Gal - 1 stimulate were 51 ± 3. 6 and 76. 7 ± 9. 07,higher than that treated with 0 μg/ mL(P < 0. 05). The number of gastric cancer cells 7 901 treated with 1and 5 μg/ mL Gal - 1 stimulate were 74. 0 ± 7. 21 and 105. 3 ± 11. 37,higher than that treated with 0 μg/ mL(P < 0. 05). The migration and invasion level were significantly increased in gastric cancer cells after Gal - 1 stimulate. The MMP - 9 expression level and active form change in gastric cancer cells were also increased after Gal - 1 stimulate. Conclusion Gal - 1cound significantly promote gastric cancer cell migration and invasion by up - regulated the MMP - 9 expression and active its enzyme activity.