Yan Wang^{1, 2}, Jichun Han¹, Xiaoyu Chen¹, Penglong Wang^{1, 3}, Wenjin Hao¹, Jun Ma¹, Bo Wang^{1, 2}, Xingjie Zhang¹, Fanqing Meng¹, Xiujuan Zhang¹, Dan Wang¹, Qiusheng Zheng^{1, 2,}

This study investigates the effects of LCA on cell-cycle distribution and glycolysis in human bladder cancer T24 cells. The mRNA expression of HIF-1α, vascular endothelial growth factor (VEGF), glucose transporter 1 (GLUT1), lactate dehydrogenase A (LDHA) and Fructose-2, 6-Biphosphatase 3 (PFKFB3) were assessed using RT-PCR. LCA elicited an anti-proliferative effect on human bladder cancer cells line T24 cells in a concentration-dependent manner; LCA induced a G2/M-phase arrest, as well as a down-regulation of the mRNA level of CDK1 and Cyclin B1; after treated with LCA, the activity of CDK1 was down regulated and the p21 was upregulated. LCA inhibited the ATP production, decreased the glucose uptake and the release of lactic acid. The activities of LDH, HK, and PK were significantly down-regulation. LCA could reduce the level of HIF-1α in T24 cells and significantly reduce the expression of its target genes: VEGF, GLUT1, LDHA and PFKFB3. This study demonstrated that LCA treatment caused a significant decrease in the proliferation and a cell cycle arrest of G2/M phase in T24 cells; the mechanism by which LCA inhibits T24 proliferation may be associated with the inhibition of glycolysis as well as cause G2/M phase arrested.

licochalcone A, T24, cell-cycle distribution, glycolysis