Salvato Ilaria, Ricciardi Luca, Nucera Francesco, Nigro Annunziata, Dal Col Jessica, Monaco Francesco, Caramori Gaetano, Stellato Cristiana
Pneumologia, Dipartimento di Scienze Biomediche, Odontoiatriche e delle Immagini Morfologiche e Funzionali (BIOMORF), Università degli Studi di Messina, Italy.
Department of Medicine, Surgery and Dentistry "Scuola Medica Salernitana", University of Salerno, Salerno, Italy.
COPD. 2023 Dec;20(1):18-30. doi: 10.1080/15412555.2022.2107500.
Chronic obstructive pulmonary disease (COPD) represents an independent risk factor for lung cancer development. Accelerated cell senescence, induced by oxidative stress and inflammation, is a common pathogenic determinant of both COPD and lung cancer. The post transcriptional regulation of genes involved in these processes is finely regulated by RNA-binding proteins (RBPs), which regulate mRNA turnover, subcellular localization, splicing and translation. Multiple pro-inflammatory mediators (including cytokines, chemokines, proteins, growth factors and others), responsible of lung microenvironment alteration, are regulated by RBPs. Several mouse models have shown the implication of RBPs in multiple mechanisms that sustain chronic inflammation and neoplastic transformation. However, further studies are required to clarify the role of RBPs in the pathogenic mechanisms shared by lung cancer and COPD, in order to identify novel biomarkers and therapeutic targets. This review will therefore focus on the studies collectively indicating the role of RBPs in oxidative stress and chronic inflammation as common pathogenic mechanisms shared by lung cancer and COPD.
慢性阻塞性肺疾病(COPD)是肺癌发生的独立危险因素。由氧化应激和炎症诱导的细胞加速衰老,是COPD和肺癌共同的常见致病决定因素。参与这些过程的基因的转录后调控受到RNA结合蛋白(RBPs)的精细调节,RBPs可调节mRNA的周转、亚细胞定位、剪接和翻译。多种促炎介质(包括细胞因子、趋化因子、蛋白质、生长因子等)负责肺微环境的改变,它们受RBPs调控。多个小鼠模型已表明RBPs参与维持慢性炎症和肿瘤转化的多种机制。然而,需要进一步研究以阐明RBPs在肺癌和COPD共同的致病机制中的作用,从而确定新的生物标志物和治疗靶点。因此,本综述将聚焦于一系列研究,这些研究共同表明RBPs在氧化应激和慢性炎症中发挥的作用,而氧化应激和慢性炎症是肺癌和COPD共有的致病机制。