Miao Guoying, Liu Baoguo, Guo Xiaohui, Zhang Xike, Liu Gui-Jing
Department of Dermatology, Affiliated Hospital of Hebei University of Engineering Handan 056029, China.
Int J Clin Exp Pathol. 2015 Jan 1;8(1):287-97. eCollection 2015.
Metformin is a biguanide widely prescribed as a first-line antidiabetic drug in type 2 diabetes mellitus patients. Animal and cellular studies support that metformin has a strong anti-proliferative effect on various cancers. Herein, we report that metformin derivative, HL010183 significantly inhibited human epidermoid A431 tumor xenograft growth in nu/nu mice, which in turn is associated with a significant reduction in proliferative biomarkers PCNA and cyclins D1/B1. Enhanced apoptotic cell death and an increase in Bax: Bcl2 ratio supported the tumor growth reduction. The mechanism of the drug effects appears to be dependent on the inhibition of nuclear factor kappa B (NFkB) and mTOR signaling pathways. Reduced enhancement of NFkB transcriptional target proteins, iNOS/COX-2 together with decreased phosphorylation of NFkB inhibitory protein IKBa were also observed. Further, AKT signaling activation was evaluated by the reduced phosphorylation at Ser473. In addition, a concomitant decrease in mTOR signaling pathway was also estimated from the reduced phosphorylation at mTOR regulatory proteins p70S6K and 4E-BP-1. Along with this, decreased phosphorylation of GSK3b, which is carried out by AKT kinases was also observed. Overall results suggested that HL010183 interrupt SCC growth via NFkB and mTOR signaling pathways.
二甲双胍是一种双胍类药物,在2型糖尿病患者中被广泛用作一线抗糖尿病药物。动物和细胞研究表明,二甲双胍对多种癌症具有强大的抗增殖作用。在此,我们报告二甲双胍衍生物HL010183能显著抑制无胸腺裸鼠体内人表皮样A431肿瘤异种移植瘤的生长,这反过来与增殖生物标志物PCNA和细胞周期蛋白D1/B1的显著减少有关。凋亡细胞死亡增加以及Bax:Bcl2比值升高支持了肿瘤生长的减少。药物作用机制似乎依赖于对核因子κB(NFkB)和mTOR信号通路的抑制。还观察到NFkB转录靶蛋白iNOS/COX-2的增强作用降低,以及NFkB抑制蛋白IKBa的磷酸化减少。此外,通过Ser473处磷酸化减少评估AKT信号激活。另外,从mTOR调节蛋白p70S6K和4E-BP-1的磷酸化减少也估计mTOR信号通路同时降低。与此同时,还观察到由AKT激酶介导的GSK3b磷酸化减少。总体结果表明,HL010183通过NFkB和mTOR信号通路中断鳞状细胞癌的生长。