Objective: To investigate the relations of DNA topoisomerase II IIα (Topo IIα) and class III β tubulin (TUBB3) expressions in breast cancer tissue with the efficacy of anthracycline- and taxane-based neoadjuvant chemotherapy. Methods: Sixty-four women with primary breast cancer were enrolled, and they were randomly designated to receive anthracycline-based regimen (20 cases), taxane-based regimen (20 cases) or anthracycline plus taxane-based regimen (24 cases) respectively, and efficacy evaluation was conducted after 3-4 cycles. The expressions of Topo IIα and TUBB3 in the needle aspiration specimens from these patients before chemotherapy were detected by immunohistochemical staining. Results: The response rate for anthracycline-based, taxane-based and combination-based regimen was 50.00%, 35.00% and 70.83% respectively, but no statistical difference was found among the three regimens (P=0.128). Patients with positive Topo IIα expression had better response to anthracycline-based regimen than those with negative Topo IIα expression (P=0.023), while the response to taxane-based regimen was not associated with Topo IIα expression status of the patients (P=0.642); patients with positive TUBB3 expression showed poorer response to taxane-based regimen than those with negative TUBB3 expression, but the difference did not reach a statistical significance (P=0.057); patients with co-positive Topo IIα and TUBB3 expression were sensitive to anthracycline-based regimen, while those with positive Topo IIα expression and negative TUBB3 expression had better response to taxane-based regimen (P=0.015); the efficacy of combination-based regimen showed no relation with either Topo IIα or TUBB3 expression status (P>0.05). Conclusion: Breast cancer patients with positive Topo IIα expression may obtain better results with anthracycline-based chemotherapy, so it may be used as a predictor for making a personalized treatment plan. However, whether TUBB3 can be used as a predictor for tailored chemotherapy still needs further investigation with larger sample size.

Objective: To observe the effects of liquiritigenin on growth, apoptosis, and autophagy of human breast carcinoma MCF-7 cells. Methods: After exposure to different concentration of liquiritigenin (0.05, 0.10, 0.20, 0.40 mmol/L) for 24, 48 and 72 h respectively, the cell viability of MCF-7 cells was determined by MTT assay. The cell apoptosis was determined by Hoechst 33342 staining and cell autophagy was observed by acridine orange (AO) staining after MCF-7 cells were exposed to liquiritigenin of above concentrations for 48 h. Results: With the increase of concentration of liquiritigenin and prolongation of exposure time, the cell viability of MCF-7 cells was gradually decreased, and some of the results reached statistical difference comparing with control (P<0.05 or P<0.01). The apoptotic rate of MCF-7 cells was increasingly elevated with the increase of concentration of liquiritigenin, and became statistically different versus control when liquiritigenin reached 0.20 mmol/L (all P<0.01). Autophagy occurred in MCF-7 cells exposed to each tested concentration of liquiritigenin, but autophagic activity presented a trend of initial increase and subsequent decrease with the increase of concentration of liquiritigenin. Conclusion: Liquiritigenin can inhibit the growth of human breast carcinoma MCF-7 cells, and this action is associated with apoptosis acceleration and autophagy induction.