Lung cancer is a leading cause of cancer-associated death worldwide [1,2]. Explanation of the molecular biology and pathogenesis of lung cancer is essential for the design of a potential treatment for patients [3,4]. Non-small-cell lung carcinoma (NSCLC) is a complex process concerning interruption of cell proliferation, cell differentiation, apoptosis and various molecular mechanisms. The abnormal expression of MAPKs is a reasonably frequent event in NSCLC. The MAPK pathway plays an important role in cell proliferation, differentiation and apoptosis [5]. Increasing evidence supports the association of MAPK signaling deregulation with various types of malignant tumors, including NSCLC. Several studies have demonstrated that members of the MAPK signaling pathway may be potential biomarkers for predicting the progression and prognosis of patients with NSCLC. Additionally, the MAPK pathway affects decisive roles in the carcinogenesis and treatment resistance of NSCLC cells by promoting proliferation or inhibiting apoptosis of NSCLC cells. In this editorial, we will focus on molecular level changes of the MAPK pathway and their therapeutic significance in NSCLC, concentrating primarily on its components which are associated with cell proliferation, cell survival or patient prognosis and potential therapy for NSCLC.
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Pradhan et al. (2019) studied this question.
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