Zhang Yu, Li Meng-Xiong, Wang Huan, Zeng Zheng, Li Xiao-Mao
Department of Gynecology The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, PR China E-mail :
Asian Pac J Cancer Prev. 2015;16(1):221-5. doi: 10.7314/apjcp.2015.16.1.221.
As metformin can inhibit endometrial carcinoma (EC) cell growth and the insulin growth factor (IGF) system is active in EC, the question of whether t can regulate endometrial carcinoma cell secretion of IGF-1 or expression of IGF-1 receptor (IGF-1R) is of interest. In this study, serum IGF-1 levels in EC patients were found to be comparable with that in the non EC patients (p>0.05). However, the IGF-1 level in the medium of cultured cells after treatment with metformin was decreased (p<0.05). IGF-1R was highly expressed in human endometrial carcinoma paraffin sections, but IGF-1R and phosphor-protein kinase B/protein kinase B (p-Akt/ Akt) expression was down-regulated after metformin treatment (p<0.05). In summary, metformin can reduce the secretion of IGF-1 by Ishikawa and JEC EC cell lines and their expression of IGF-1R to deactivate downstream signaling involving the PI-3K/Akt pathway to inhibit endometrial carcinoma cell growth.
由于二甲双胍可抑制子宫内膜癌（EC）细胞生长，且胰岛素生长因子（IGF）系统在EC中具有活性，因此二甲双胍是否能调节子宫内膜癌细胞分泌IGF-1或IGF-1受体（IGF-1R）的表达这一问题备受关注。在本研究中，发现EC患者的血清IGF-1水平与非EC患者相当（p>0.05）。然而，用二甲双胍处理后，培养细胞培养基中的IGF-1水平降低（p<0.05）。IGF-1R在人子宫内膜癌石蜡切片中高表达，但二甲双胍处理后IGF-1R和磷酸化蛋白激酶B/蛋白激酶B（p-Akt/Akt）表达下调（p<0.05）。总之，二甲双胍可降低Ishikawa和JEC EC细胞系中IGF-1的分泌及其IGF-1R的表达，使涉及PI-3K/Akt途径的下游信号失活，从而抑制子宫内膜癌细胞生长。
