Regulatory effect of strengthening qi and nourishing yin recipe on expressions of ERα and CyclinD1 of Lewis lung cancer in C57 mice

Objective: To observe the effect of strengthening qi and nourishing yin recipe (SQNY recipe) on the expressions of estrogen receptor α (ERα) and CyclinD1 of Lewis lung cancer in C57BL/6 mice with immunohistochemistry, and discuss the mechanism of its anti-proliferation and anti-metastasis effects, and analyse the correlation between ERα and CyclinD1. Methods: Twenty-four C57BL/6 mice were randomly divided into three groups. They were all transplanted with Lewis lung cancer cells, and received the interventions the next day as follows: tumor-bearing control group was fed with 0.9% NaCl, and TCM group was treated with SQNY recipe, and DDP group was given intraperitoneal DDP injection. All of mice were killed on the 20th day, weighed the tumor and counted lung metastases to calculate the inhibition rates of tumor growth and metastasis. The expressions of ERα, CyclinD1 in tumor tissues were detected by immunohistochemistry. Results: The inhibition rates of tumor growth and metastasis were 35.02% and 54.20% in TCM group, and were 41.18% and 39.02% in DDP group, respectively (all P0.05). The positive rates of ERα and CyclinD1 were 100% and 75% respectively in tumor-bearing group, all significantly higher than those in TCM group and DDP group (all P0.05). The expressions of ERα and CyclinD1 were all positively correlated to the tumor-weight (rs=0.501 and 0.404 respectively, both P0.05)and metastasis (rs=0.605 and 0.535 respectively, both P0.01). ERα was also positively correlated to CyclinD1 (rs=0.542,P0.01). Conclusion: SQNY recipe had good and ideal effects on tumor-inhibition and anti-metastasis, and can significantly regulate down the expressions of ERα and CyclinD1 in lung cancer, which was one of the mechanisms in anti-proliferation and anti-metastasis effects of this recipe. ERα and CyclinD1 in lung cancer were highly expressed, which was the critical reason and judging index of promoting the proliferation and metastasis of lung cancer cells. There was a regulatory mechanism between the expressions of ERα and CyclinD1.