目的： 探讨过表达血管生成抑制蛋白1（vasohibin-1，VASH1）对人结直肠癌细胞恶性生物学行为的影响。方法： 包装慢病毒并感染人结直肠癌SW680、SW620细胞以构建过表达VASH1的细胞系，以未经感染的细胞为对照；qPCR实验和WB实验检测VASH1的过表达效果，小管形成实验、CCK-8实验、软琼脂克隆形成实验、Transwell实验和划痕愈合实验检测过表达VASH1在体外对细胞的微血管形成、增殖、克隆形成以及迁移能力的影响，NOD-SCID小鼠皮下成瘤实验检测过表达VASH1对SW620细胞移植瘤的体内生长和肺转移的影响。结果： 成功构建过表达VASH1的SW480和SW620细胞。体外实验表明，与对照组相比，过表达VASH1的结直肠癌细胞的微血管形成能力、增殖能力、克隆形成能力以及迁移能力均显著降低（均P<0.05）。体内实验表明，与对照组相比，过表达VASH1的SW620细胞NOD-SCID小鼠皮下移植瘤的生长速度以及肺转移能力也明显降低（均P<0.05）。结论： 过表达VASH1能够抑制人结直肠癌细胞的恶性生物学行为。

Objective: To investigate the effects of over-expressing VASH1 on the malignant biological behaviors of human colorectal cancer cells.Methods: Lentivirus was packaged and transfected into human colorectal cancer cells SW680 and SW620 to construct an over-expressed VASH1 cell line, the untransfected cells were used as control. qPCR experiment and WB experiment were used to detect the over-expression effect of VASH1. The effects of VASH1 over-expressed on microangiogenesis, proliferation, colony formation and migration of colorectal cancer cells were detected respectively by tubule formation, CCK-8 assay, soft agar assay, Transwell assay and Wound healing assay in vitro. In addition, tumor growth and lung metastasis were detected in NOD-SCID mice subcutaneously injected with VASH1-overexpressing SW620 cells.Results: Successfully constructed SW480 and SW620 cells over-expressing VASH1. Compared with the control group, the abilities of microangiogenesis, proliferation, colony forming and migration were significantly reduced in colorectal cancer cells over-expressing VASH1 (P<0.05) in vitro. The abilities of subcutaneous tumor growth and lung metastasis of colorectal cancer cells over-expressing VASH1 were also significantly reduced (P<0.05) in vivo.Conclusion: Over-expression of VASH1 can suppress the malignant biological behaviors of human colorectal cancer cells.

R735.3; R730.54

天津市卫生健康委员会项目资助（No. 2014KZ053，No. 2017057）；天津市科技支撑重点研发计划项目资助（No. 19YFZCSY00420）；南开大学国家重点实验室开放课题资助项目（No. 2018094）；天津市重大疾病防治科技重大专项资助项目（No. 18ZXDBSY00040）；天津市人民医院院级课题资助项目（No. 2016YJ035）