Abstract
Lung cancer represents a genetically heterogeneous disease with low survival rates. Recent data have evidenced key roles of noncoding RNAs in lung cancer initiation and progression. These functional RNA molecules that can act as both oncogenes and tumor suppressors may become future biomarkers and more efficient therapeutic targets. In the precision medicine era, circulating nucleic acids have the potential to reshape the management and prognosis of cancer patients. Detecting genomic alterations and level variations of circulating nucleic acids in liquid biopsy samples represents a noninvasive method for portraying tumor burden. Research is currently trying to validate the potential role of liquid biopsy in lung cancer screening, prognosis, monitoring of disease progression, and treatment response. However, this method requires complex detection assays, and implementation of plasma genotyping in clinical practice continues to be hindered by discrepancies that arise when compared to tissue genotyping. Understanding the genomic landscape of lung cancer is essential in order to provide useful and innovative research in the age of patient-tailored therapy. In this landscape, the noncoding RNAs play a crucial role due to their target genes that dramatically influence the tumor microenvironment and the response to therapy. This article addresses present and future possible roles of liquid biopsy in lung cancer. It also discusses how the complex role of noncoding RNAs in lung tumorigenesis could influence the management of this pathology.
Highlights
Lung cancer represents the most frequently diagnosed and the leading cause of cancer-related death in males on a global level
Recent data report a branched evolution of non-small-cell lung cancer (NSCLC) with heterogeneous mutations that develop in response to local environmental factors [15]
Two of the miRNAs involved in cell cycle arrest and cell senescence in lung cancer are miR-641 and miR-660 that target MDM2, a suppressor of p53 pathway [55,58]. miRNAs, such as the miR-200 family, have been discovered to play a role in the complex invasion–metastasis process in lung cancer, at the center of which lies the epithelial-to-mesenchymal transition (EMT), characterized by increased cell motility caused by the loss of cell adhesion mediated by E-cadherin [59]
Summary
Antonia Harangus, 1,2 , Ioana Berindan-Neagoe 1,3,4 , Doina Adina Todea 2,5 , Ioan S, imon 6, * and Mărioara S, imon 2. MEDFUTURE-Research Center for Advanced Medicine, Iuliu Hatieganu University of Medicine and Pharmacy, 23 Marinescu Street, 400337 Cluj-Napoca, Romania. Departament of Pulmonology, Iuliu Hat, ieganu University of Medicine and Pharmacy, 40037 Cluj Napoca, Romania. Departament of Surgery, Iuliu Hat, ieganu University of Medicine and Pharmacy, 40037 Cluj Napoca, Romania. Received: 20 October 2019; Accepted: 4 December 2019; Published: 9 December 2019
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