Objective: To investigate the anti-proliferation effect of licochalcone B (LCB) on the breast cancer MCF-7 cells

and discuss its action mechanism. Method: MCF-7 cells in logarithmic growth phase were inoculated into 6-well plates at a density of 6×104 cells/well; then Trypan blue staining was performed to obtain the cell growth curve and calculate cell doubling time. MCF-7 cells in logarithmic growth phase were inoculated into 96-well plates at a density of 1×104 cells/well; then MTT assay was used to detect the anti-proliferation effect of LCB (0

10

20

40

60

80 μmol·L-1) after treatment for 24

48

72 h. MCF-7 cells in logarithmic growth phase were inoculated into 6-well plates at a density of 2×105 cells/well; then the morphological changes of MCF-7 cells were observed under microscope after 48 h treatment by LCB (0

20

40

80 μmol·L-1). MCF-7 cells in logarithmic growth phase were inoculated into 6-well plates at a density of 2×105 cells/well; then the morphology of apoptosis was observed by Hoechst 33258 staining method. MCF-7 cells in logarithmic growth phase were inoculated into cell culture flask at a density of 9×105 cells/flask; then after 48 h treatment by LCB (0

20

40

80 μmol·L-1)

apoptosis rate was determined by flow cytometry

and real-time fluorescence quantitative polymerase chain reaction (qPCR) method was used to detect the changes in Bcl-XL

Bax

Caspase-3 and Caspase-9 transcriptional levels. Result: As compared with 0 μmol·L-1 group

LCB effectively inhibited MCF-7 cell lines proliferation in a concentration-dependent and time-dependent manner; LCB treatment increased apoptosis rate of MCF-7 with obvious morphological changes

exhibiting chromosomes margination

nuclear condensation

nuclear fragmentation and other morphological features. Cell apoptosis induced by licochalcone B exhibited a concentration-dependent manner; licochalcone B significantly down-regulated the expression levels of Bcl-XL and up-regulated the expression levels of Bax

Caspase-3 and Caspase-9 (P<0.05

P<0.01). Conclusion: LCB could significantly inhibit proliferation and induce apoptosis of breast cancer MCF-7 cells

and the mechanism may be associated with up-regulating Bax

down-regulating Bcl-XL expression levels

and activating Caspase-3/Caspase-9-mediated mitochondrial apoptosis signaling pathways.