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目的研究巨噬细胞刺激蛋白受体(MST1R)过表达对结肠癌细胞侵袭能力的影响。方法将携有野生型 MST1R(wt-MST1R)cDNA 的质粒 pDR2-wt-MST1R 转染入结肠癌细胞株 RKO,挑选稳定转染克隆。以过河实验和趋化运动实验检测二者的移动能力,以基质浸润实验检测浸润能力,以 Western 印迹检测 E-钙粘连蛋白表达的变化。结果转染并高表达 wt-MST1R 后,RKO 细胞的趋化移动能力明显增加(P<0.01)。过河实验中转染组过河时间为(42.50±4.12)h,而未转染组与载体对照组分别为(69.50±2.52)h 与(70.50±3.42)h(P<0.01)。基质浸润实验中转染组47.90±6.82/视野,未转染组与载体对照组分别为25.90±4,56/视野与26.50±5.36/视野(P<0.01)。转染wt-MST1R 后,E-钙粘连蛋白表达降低(P<0.05)。结论 wt-MST1R 高表达可降低 E-钙粘连蛋白表达,降低肿瘤细胞间的黏附性,增加结肠癌细胞株 RKO 的侵袭能力。提示 MST1R 高表达可能是结肠癌的浸润转移机制之一。
Objective To investigate the effect of macrophage stimulating protein receptor (MST1R) overexpression on invasion of colon cancer cells. Methods The plasmid pDR2-wt-MST1R carrying the wild-type MST1R (wt-MST1R) cDNA was transfected into the colon cancer cell line RKO and the stable transfected clones were selected. The cross-river experiment and chemotactic experiment were used to test the mobility of the two. The infiltration ability was detected by matrix infiltration test and the expression of E-cadherin was detected by Western blotting. Results After transfected with wt-MST1R, the chemotactic ability of RKO cells increased significantly (P <0.01). The cross-river crossing time was (42.50 ± 4.12) h in the trans-river experiment, while it was (69.50 ± 2.52) h and (70.50 ± 3.42) h in the untransfected and control groups (P <0.01). In the matrix infiltration experiment, the transfection group was 47.90 ± 6.82 per field, and the non-transfected group and vehicle control group were 25.90 ± 4,56 / field and 26.50 ± 5.36 / field respectively (P <0.01). E-cadherin expression decreased after transfection of wt-MST1R (P <0.05). Conclusion High expression of wt-MST1R can reduce the expression of E-cadherin, reduce the adhesion between tumor cells and increase the invasiveness of colon cancer cell line RKO. Tip MST1R high expression may be one of the mechanisms of invasion and metastasis of colon cancer.