Effects of Insulin-like Growth Factor 1 Receptor and Its Inhibitor AG1024 on the Progress of Lung Cancer

作     者：魏艳红 唐和孝 廖永德 付圣灵 徐利强 陈广 张超 具晟 刘昭国 游良坤 喻莉 周晟 

作者机构：Department of Nephrology Union Hospital Tongji Medical College Huazhong University of Science and Technology Department of Thoracic Surgery Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Department of Intensive Care Unit Wuhan Central Hospital Tongji Medical College Huazhong University of Science and Technology Department of Thoracic Surgery Taihe Hospital Hubei University of Medicine Department of Respiratory Medicine the Central Hospital of Yichang Department of Thoracic Surgery Zhejiang Hospital Department of Pathology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology 

出 版 物：《Journal of Huazhong University of Science and Technology(Medical Sciences)》 (华中科技大学学报（医学英德文版）)

年 卷 期：2015年第35卷第6期

页      面：834-841页

核心收录：

学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

基　　金：supported by grants from the Young Science Foundation of Wuhan Central Hospital(No.YQ15A01) the National Natural Science Foundation of China(No.81501985 and No.81272590) 

主　　题：lung cancer mouse lung adenocarcinoma model insulin-like growth factor-1 receptor AG 1024 

摘      要：Summary： The type 1 insulin-like growth factor receptor （IGF-1R） and its downstream signaling com- ponents have been increasingly recognized to drive the development of malignancies, including non-small cell lung cancer （NSCLC）. This study aimed to investigate the effects of IGF-1R and its in- hibitor, AG1024, on the progression of lung cancer. Tissue microarray and immunohistochemistry were employed to detect the expressions of IGF-1 and IGF-1R in NSCLC tissues （n=198）. Western blotting was used to determine the expressions oflGF-1 and phosphorylated IGF-1R （p-IGF-1R） in A549 human lung carcinoma cells, and MTT assay to measure cell proliferation. Additionally, the expressions of IGF-1, p-IGF-1R and IGF-1R in a mouse model of lung cancer were detected by Western blotting and real-time fluorescence quantitative polymerase chain reaction （FQ-PCR）, respectively. The results showed that IGF-1 and IGF-1R were overexpressed in NSCLC tissues. The expression levels of IGF-1 and p-IGF-1R were significantly increased in A549 cells treated with IGF-1 as compared to those treated with IGF-1 ＋AG 1024 or untreated cells. In the presence of IGF-1, the proliferation of A549 cells was significantly increased. The progression of lung cancer in mice treated with IGF-1 was significantly increased as compared to the group treated with IGF-l＋AG1024 or the control group, with the same trend mirrored in IGF-1/p-IGF-1R/IGF-1R at the protein and/or mRNA levels. It was concluded that IGF- 1 and IGF inhibitor AG 1024 promotes lung cancer progression.