OBJECTIVE: To explore the effects of simvastatin on tumor growth

blood coagulation in mice with colorectal cancer based on microRNA（miR）-181/nuclear factor（NF）-κB pathway. METHODS: The colorectal cancer mice model was established by subcutaneous injection of human colorectal cancer cell line SW480

and 30 model mice were randomly divided into the control group

simvastatin low-dose group and simvastatin high-dose group. The simvastatin low-dose group and simvastatin high-dose group were intraperitoneally injected with 50 mg/kg and 100 mg/kg simvastatin

qd. On the 28 th day

tumor growth

angiogenesis

coagulation indicators were analyzed. The expression levels of miR-181

IκBα and NF-κB mRNA and protein in tumor tissues were detected by quantitative reverse transcription polymerase chain reaction and western blotting. RESULTS: Compared with the control group

the tumor volume

mass

CyclinD1 protein

Ki67 protein

Bcl-2 protein

microvessel density

vascular endothelial growth factor（VEGF） levels

whole blood viscosity

IκBα and NF-κB mRNA and protein expression levels of the simvastatin low-dose group and simvastatin high-dose group decreased significantly

while Bax protein and miR-181 levels increased

plasma prothrombin time（PT）

activated partial thromboplastin time（APTT） and miR-181 were prolonged significantly

with statistically significant differences（P<0.05）. The tumor volume

mass and microvascular density in simvastatin high-dose group were significantly lower than those in simvastatin low-dose group [（171.74±19.33） mm~3 vs.（226.52±26.38） mm~3

（0.21±0.03） g vs.（0.28±0.04）g

（9.77±1.85）% vs.（16.39±2.11）%]

CyclinD1

Ki67 and Bcl-2 protein levels

VEGF levels

whole blood viscosity

expression levels of IκBα and NF-κB mRNA and protein were significantly lower than those in simvastatin low-dose group; the levels of Bax protein and miR-181 were significantly higher than those of simvastatin low-dose group

PT and APTT were significantly longer than those of simvastatin low-dose group

the differences were statistically significant（P<0.05）. CONCLUSIONS: Simvastatin may inhibit tumor growth and angiogenesis in colorectal cancer model mice by regulating the miR-181/NF-κB pathway

and alleviate blood hypercoagulability.