Mechanism of Ginsenoside Rh1 in Regulating Breast Cancer Cell Extravasation Based on CCL20-CCR6

Abstract

Objective: To explore the regulatory mechanism of ginsenoside Rh1 on breast cancer cell extravasation based on CCL20-CCR6. Methods: In 2021, a total of 34 patients with breast cancer were treated in Baoding First Central Hospital. During hospitalization, pathological examinations were performed, and all the patients were diagnosed with invasive ductal carcinoma. Out of the 34 cases, 16 cases were found to have CCR6 expression in breast cancer tissues, in which they were recorded as the CCR6 expression group, whereas 18 cases did not have CCR6 expression; these cases were recorded as the CCR6 non-expression group. During the same period, 21 normal patients were selected as the control group. The peripheral blood CCL20 level and the expression of CCR6 on the surface of CD3+ T lymphocytes were analyzed. The extracts of cancer cells were collected, purified, and cultured, and the effect of ginsenoside Rh1 on the invasion and metastasis of breast cancer cells was analyzed. Results: The peripheral blood CCL20 level in the CCR6 expression group was significantly higher than that in the CCR6 non-expression group and the control group, in which p < 0.05, indicating that the difference was statistically significant; at 12, 24, and 48 hours, the cell survival rate of each dose group was significantly higher than that of the blank control group and the dimethyl sulfoxide (DMSO) group (p < 0.05). At 48 hours, comparing the low-dose group with the high-dose group, the cell survival rate significantly decreased (p < 0.05). Compared with the blank control group and DMSO group, the invasion ability of breast cancer cells could be reduced in both, high- and medium-dose groups, where p < 0.05, indicating that the difference was statistically significant. Conclusion: CCL20 may play a role in the pathogenesis of certain breast cancers, and ginsenoside Rh1 can effectively regulate the invasion and migration of breast cancer cells.