目的： 探讨FBXW7基因点突变对结直肠癌细胞株HCT-116增殖、凋亡、迁移和侵袭的影响。 方法： 通过构建FBXW7 基因野生型及突变型过表达的重组载体，并将其转染HCT-116细胞，应用Western blotting检测转染后FBXW7蛋白表达情况。 CCK-8检测细胞增殖能力,平板细胞克隆形成实验(HTCA)检测肿瘤细胞克隆形成能力,流式细胞术检测细胞凋亡情况,划痕及 Transwell细胞迁移实验检测细胞迁移和侵袭能力。 结果： 转染野生型FBXW7基因的HCT-116细胞中FBXW7蛋白表达水平高 于对照组（转染突变型FBXW7基因的HCT-116细胞）、阴性对照组（转染空质粒载体pEZ-M90的HCT-116细胞）及空白对照组（未 进行任何特殊处理的HCT-116细胞） （均P<0.05）。转染野生型FBXW7的HCT-116细胞的增殖、克隆形成、迁移和侵袭能力相较 于其余各组均显著下降（均P<0.05），且细胞凋亡率显著升高（P<0.05）。 结论： FBXW7基因点突变可使其蛋白表达水平降低，从 而促进结直肠癌HCT-116细胞的增殖、迁移和侵袭，并抑制其凋亡。

Objective: To investigate the impact of FBXW7 gene mutation on cell proliferation, apoptosis, migration, and invasion pro- cesses of colorectal cancer HCT-116 cell line. Methods: Recombinant plasmids carrying wild-type and mutant-type FBXW7 SNP were constructed and transfected into HCT-116 cell line; the FBXW7 protein expression level in HCT-116 strains after transfection was de- tected by Western blotting. Subsequently, cell proliferation capacity was tested by CCK-8 assay; tumor cell colony formation ability was tested by HTCA; cell apoptosis function was tested by FCM; cell migration and invasion were tested by scratch assay and Tran- swell assay, respectively. Results: Higher HBXW7 protein expression level was detected in HCT-116 strain transfected with wild-type HBXW7 in comparison to the control group (strains transfected with mutant-type HBXW7), negative-control (strains transfected with empty plasmids), and blank-control (strains untransfected) (all P<0.05). Compared with the other groups, strains transfected with wild- type HBXW7 exhibited significantly reduced proliferation, colony formation, migration and invasion ability (all P<0.05), but obviously increased apoptosis rate (P<0.05). Conclusion： ：FBXW7 gene mutation can down-regulate its protein expression, and further promote the proliferation, migration and invasion as well as inhibit the apoptosis of HCT-116 cells.

重庆市科委自然科学基金项目(No. cstc2012jjA10038)