OBJECTIVE: To probe into the effects of apatinib on tumor inhibition rate and tumor cell apoptosis in breast cancer mouse model by regulating extracellular regulated kinase（ERK） 1/2 pathway. METHODS: Human breast cancer cell line MCF-7 cells were inoculated in the right chest wall of nude mice

which were randomly divided into control group

low-dose group[10 mg/（kg·d） of Apatinib] and high-dose group[30 mg/（kg·d） of Apatinib]

after successful modeling

with 12 mice in each group. After intragastric administration once a day for 21 days

the tumor growth curves of three groups were plotted and the tumor inhibition rates were compared. After the last administration

the mice were executed and the tumor tissues were collected

the expression of ERK1/2 pathway-related proteins [ERK1/2

phosphorylated ERK1/2（p-ERK1/2）] in the tumor tissues was detected by Western blot. The effects of apatinib on MCF-7 cell cycle distribution and cell apoptosis were detected by flow cytometry. RESULTS: After processing with different concentrations of apatinib

the differences in apoptosis rate and the proportion of MCF-7 cells distributed in G

0

-G

1

phase were statistically significant（P

<

0.05）

among which the apoptosis rate and the proportion of MCF-7 cells distributed in G

0

-G

1

phase were significantly higher in the group given 20 μmol/L of apatinib than in the other low concentration groups

with statistically significant differences（P

<

0.05）. The tumor volumes of mice in the high-dose and low-dose groups were significantly lower than that of the control group at the 6 th to 21 st day of administration

with statistically significant differences（P

<

0.05）

of which the tumor volumes of mice in the high-dose group were the smallest. The mean tumor weights of the high-dose group and low-dose group on the 22 nd day were respectively（0.343±0.089） g and（0.658±0.145） g

which were significantly lower than that of the control group[（1.163±0.231） g]

with statistically significant differences（P

<

0.05）. The tumor inhibition rates of the high-dose group and low-dose group were respectively 64.46% and 34.07%

and there was a dose dependence. The expression levels of ERK1/2 and p-ERK1/2 in mice in the high-dose group and low-dose group were significantly lower than those in the control group

with statistically significant difference（P

<

0.05）

of which the expression levels of ERK1/2 and p-ERK1/2 in mice in the high-dose group were the lowest. CONCLUSIONS: Apatinib can effectively inhibit the ERK1/2 signaling pathway in breast cancer cell

induce apoptosis and proliferation of tumor cells

and thus inhibit the growth of tumors in breast cancer mice.