作者: Ji-Ching Lai , Ya-Wen Cheng , Hui-Ling Chiou , Ming-Fang Wu , Chin-Yi Chen
DOI: 10.1002/IJC.21278
关键词: Estrogen receptor alpha 、 Estrogen receptor 、 Endocrinology 、 Internal medicine 、 Respiratory disease 、 DNA methylation 、 Prostate 、 Carcinogenesis 、 Medicine 、 Tumor progression 、 Lung cancer 、 Cancer research
摘要: It has been documented that estrogen receptor (ER) transcription silencing due to hypermethylation is linked the tumor progression of breast, uterine and prostate cancers. Additionally, ER in lung tumors associated with exposure specific carcinogens animal study. The role hypermethylation-induced its prognostic value for non-small cell cancer (NSCLC) patients remained unclear. In our study, 123 adjacent normal parts were examined by methylation-specific PCR (MSP). Estrogen mRNA expression was determined RT-PCR. Our data indicated only detected tumors, but not tissues. This suggests may be tumorigenesis. Among clinical parameters studied, gender factor correlated a higher frequency being male than female (58 vs. 34%, p = 0.01). After stratified cigarette smoking status, similarly high prevalence found nonsmoking (60 61%) as compared (34%). To investigate if 17-beta estradiol (E2) responsible such difference hypermethylation, A549 without treated E2 various concentrations defined time intervals show an treatment could restore eliminate hypermethylation. Western blot also showed acetylated histone 3 4 chromatin increased significantly treatment. Thus, can make re-expression eliminating elucidate Kaplan-Meier analysis carried out had poorer prognosis those Such prediction, however, applied (p 0.0044) patients. Cox regression further feasibility independent NSCLC 0.007). possible antiestrogens have different therapeutic values