The inhibitory effect of Licochalcone B on the triple negative breast cancer cell MDA-MB-231 and its mechanism
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Abstract:
Objective: To investigate the inhibitory effect of Licochalcone B (LCB) on a triple-negative breast cancer cell line MDA-MB-231 cells and its mechanism. Methods: MDA-MB-231 cells were routinely cultured and treated with different concentrations of LCB, and then CCK-8 assay, immunofluorescence, FCM and WB analysis were used to detect the proliferative viability of MDA-MB-231 cells, the expression of γ-H2AX, a marker of DNA double-strand breaks in the nucleus, the cell cycle,and the expression levels of proteins related to cycle regulation, mitogen-activated protein kinase (MAPK), and the endoplasmic reticulum stress (ER stress),respectively. Results: LCB significantly inhibited the proliferative viability of breast cancer MDA-MB-231 cells (all P<0.05), the number of γ-H2AX-positive cells and protein expression levels were significantly increased after LCB treatment (all P<0.05), the number of cells in G2/M and S phases was significantly increased (all P<0.05), the phosphorylation levels of the main members of the MAPK family,extracellular regulated kinase 1/2 (ERK1/2) and p38 MAPK phosphorylation levels were significantly upregulated (all P<0.05), and the expression of ER stress pathway-related proteins Bip, ATF4 and CHOP were significantly upregulated (all P<0.05). Conclusion: LCB could significantly inhibit the proliferation vitality of MDA-MB-231 cells and induce DNA damage and cell cycle arrest at G2/M and S phases.The inhibitory effect of LCB on MDA-MB-231 cells may be related to the activation of MAPK and ER stress signaling pathway.