作者: Mercè Mateu-Jimenez , Víctor Curull , Alberto Rodríguez-Fuster , Rafael Aguiló , Albert Sánchez-Font
DOI: 10.1186/S13148-017-0437-0
关键词: Medicine 、 PTEN 、 Cancer research 、 Carcinogenesis 、 Epigenomics 、 Lung cancer 、 Respiratory disease 、 Tumor progression 、 DNA methylation 、 Lung
摘要: Chronic lung diseases such as chronic obstructive pulmonary disease (COPD) and epigenetic events underlie cancer (LC) development. The study objective was that tumor expression levels of specific microRNAs their downstream biomarkers may be differentially regulated in patients with without COPD. In specimens (tumor non-tumor), known to involved tumorigenesis (miR-21, miR-200b, miR-126, miR-451, miR-210, miR-let7c, miR-30a-30p, miR-155 miR-let7a, qRT-PCR), DNA methylation, were determined (qRT-PCR immunoblotting) 40 LC (prospective study, subdivided into LC-COPD LC, N = 20/group). Expression miR-21, miR-let7c methylation greater than patients. markers PTEN, MARCKs, TPM-1, PDCD4, SPRY-2, ETS-1, ZEB-2, FGFRL-1, EFNA-3, k-RAS together P53 selectively downregulated samples these patients, miR-126 miR-451 the SNAIL-1, P63, reduced. Biomarkers mechanisms growth, angiogenesis, migration, apoptosis expressed tumors underlying respiratory disease. These findings shed light biology reported risk develop seen conditions. presence an should identified all differential biological profile help determine progression therapeutic response. Additionally, offer a niche for pharmacological targets.