Heng Zhang1, Chunfang Zhang1, Dongkai Wu2. 1. Department of Cardiothoracic Surgery, Xiangya Hospital of Central South University, No.87, Xiangya Road, Kaifu District, HuNan, ChangSha 410008, China. 2. Department of Cardiothoracic Surgery, Xiangya Hospital of Central South University, No.87, Xiangya Road, Kaifu District, HuNan, ChangSha 410008, China. Electronic address: dongkairwu@outlook.com.
Abstract
BACKGROUND AND AIMS: The prevalence of lung cancer is increasing in the recent decades. The underlying mechanism is unclear. The insulin-like growth factor (IGF) and p53 protein are important molecules involving the tumor immunity. This study aims to investigate the role of IGF intervene the radiation-induced lung cancer apoptosis. METHODS: Lung cancer cells were isolated from surgically removed lung cancer tissue. The lung cancer cell lines, A549 cells and H23 cells were irradiated. The expression of IGF1 receptor (IGF1R) by the lung cancer cells, and apoptosis, were assessed by flow cytometry. RESULTS: The results showed that human lung cancer cells expressed IGF1R. IGF1R played a critical role in the radiation-induced lung cancer cell apoptosis. The histone deacetylase-1 (HDAC1) phosphorylation was up regulated by irradiation. The phosphorylated HDAC1 bound the p53 promoter to inhibit the gene transcription, which was abolished by the presence of an inhibitor of HDAC1 or a STAT3 inhibitor. CONCLUSION: The data suggest that activation of IGF1R plays a critical role in the radioresistance, which can be prevented in the presence of the inhibitors of HDAC1 or STAT3 inhibitors.
BACKGROUND AND AIMS: The prevalence of lung cancer is increasing in the recent decades. The underlying mechanism is unclear. The insulin-like growth factor (IGF) and p53 protein are important molecules involving the tumor immunity. This study aims to investigate the role of IGF intervene the radiation-induced lung cancer apoptosis. METHODS:Lung cancer cells were isolated from surgically removed lung cancer tissue. The lung cancer cell lines, A549 cells and H23 cells were irradiated. The expression of IGF1 receptor (IGF1R) by the lung cancer cells, and apoptosis, were assessed by flow cytometry. RESULTS: The results showed that humanlung cancer cells expressed IGF1R. IGF1R played a critical role in the radiation-induced lung cancer cell apoptosis. The histone deacetylase-1 (HDAC1) phosphorylation was up regulated by irradiation. The phosphorylated HDAC1 bound the p53 promoter to inhibit the gene transcription, which was abolished by the presence of an inhibitor of HDAC1 or a STAT3 inhibitor. CONCLUSION: The data suggest that activation of IGF1R plays a critical role in the radioresistance, which can be prevented in the presence of the inhibitors of HDAC1 or STAT3 inhibitors.
Authors: Irasema Oroz-Parra; Mario Navarro; Karla E Cervantes-Luevano; Carolina Álvarez-Delgado; Guy Salvesen; Liliana N Sanchez-Campos; Alexei F Licea-Navarro Journal: Toxins (Basel) Date: 2016-02-05 Impact factor: 4.546
Authors: Julio Cesar M de-Freitas-Junior; Jéssica Andrade-da-Costa; Mariana Costa Silva; Salomé S Pinho Journal: Int J Mol Sci Date: 2017-09-07 Impact factor: 5.923