Abstract
Lung cancer represents the primary cause of cancer death in the world. Malignant cells identification and characterization are crucial for the diagnosis and management of patients with primary or metastatic cancers. In this context, the identification of new biomarkers is essential to improve the differential diagnosis between cancer subtypes, to select the most appropriate therapy, and to establish prognostic correlations. Nuclear abnormalities are hallmarks of carcinoma cells and are used as cytological diagnostic criteria of malignancy. Lamins (divided into A- and B-types) are localized in the nuclear matrix comprising nuclear lamina, where they act as scaffolding protein, involved in many nuclear functions, with regulatory effects on the cell cycle and differentiation, senescence and apoptosis. Previous studies have suggested that lamins are involved in tumor development and progression with opposite results concerning their prognostic role. This review provides an overview of lamins expression in lung cancer and the relevance of these findings for disease diagnosis and prognosis. Furthermore, we discuss the link between A-type lamins expression in lung carcinoma cells and nuclear deformability, epithelial to mesenchymal transition, and metastatic potential, and which mechanisms could regulate A-type lamins expression in lung cancer, such as the microRNA miR-9.
Highlights
Lung cancer is one of the most frequent cancers and the leading cause of cancer-related mortality in developed countries [1,2]
According to Kaufmann’s study, lamin A and C expression was reduced of more than 80% in small cell lung cancer (SCLC) cell lines compared to non-small cell lung cancer (NSCLC) cell lines, using Western and Northern Blotting [46]
Pajerowski et al demonstrated that the loss of A-type lamins in lung adenocarcinoma cell line A549 enhanced their nuclear deformability compared to A549 cells expressing these lamins [57]
Summary
Lung cancer is one of the most frequent cancers and the leading cause of cancer-related mortality in developed countries [1,2]. A, including the cleavage site of FACE1/ZMPSTE24 protease, resulting in the abnormal persistence of a C-terminal farnesylated cysteine at the end of the maturation processing [32,33] This abnormal protein, called ‘progerin’, remains anchored in the INM, generating nuclear abnormalities and severe nuclear dysfunctions leading to a premature senescence. An enhanced expression of A-type lamins was associated with higher stage tumors or a decreased overall survival (Table 1) These results showed that the role of lamins A and C is probably dependent of the context and cancer type and requires other studies to identify their role in the progression of cancer, according to the histological type, the mutational profile and the stage of the underlying disease. We discuss lamins expression variations in lung cancer, the impact of these findings for disease diagnosis and prognosis and which mechanisms could regulate A-type lamins expression in lung cancer, such as the microRNA miR-9
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