Gene-expression profiles in lung adenocarcinomas related to chronic wood smoke or tobacco exposure. Issue 1 (December 2016)

• Record Type: Journal Article
• Authors: Ortega-Gómez, Alette; Rangel-Escareño, Claudia; Molina-Romero, Camilo; Macedo-Pérez, Eleazar; Avilés-Salas, Alejandro; Lara-García, Alejandra; Alanis-Funes, Gerardo; Rodríguez-Bautista, Rubén; Hidalgo-Miranda, Alfredo; Arrieta, Oscar
• Is Part Of: Respiratory research. Volume 17:Issue 1(2016)
• Page Start: 1
• Page End: 14
• Publication Date: 2016-12
• Subjects: Non-small cell lung carcinoma -- Wood smoke exposure -- Gene expression profiles -- Tobacco smoke -- Microarray analysis; Respiratory organs -- Diseases -- Periodicals; 616.2005
• DOI: 10.1186/s12931-016-0346-3
• Languages: English
• ISSNs: 1465-993X

Abstract

Abstract Background Tobacco-smoke is the major etiological factor related to lung cancer. However, other important factor is chronic wood smoke exposure (WSE). Approximately 30 % of lung cancer patients in Mexico have a history of WSE, and present different clinical, pathological and molecular characteristics compared to tobacco related lung cancer, including differences in mutational profiles. There are several molecular alterations identified in WSE associated lung cancer, however most studies have focused on the analysis of changes in several pathogenesis related proteins. Methods Our group evaluated gene expression profiles of primary lung adenocarcinoma, from patients with history of WSE or tobacco exposure. Differential expression between these two groups were studied through gene expression microarrays. Results Results of the gene expression profiling revealed 57 statistically significant genes (p < 0.01). The associated biological functional pathways included: lipid metabolism, biochemistry of small molecules, molecular transport, cell morphology, function and maintenance. A highlight of our analysis is that three of the main functional networks represent 37 differentially expressed genes out of the 57 found. These hubs are related with ubiquitin C, GABA(A) receptor-associated like protein; and thePI3K/AKT andMEK/ERK signaling pathways. Conclusion Our results reflect the intrinsic biology that sustains the development of adenocarcinoma related to WSE and show that there is a different gene expression profile of WSE associated lung adenocarcinoma compared to tobacco exposure, suggesting that they arise through different carcinogenic mechanisms, which may explain the clinical and mutation profile divergences between both lung adenocarcinomas.