Multiple mutations of lung squamous cell carcinoma shared common mechanisms

// Qianping Li 1, * , Junyi Hou 2, * , Zhaoyan Hu 3 , Biao Gu 4 , Yan Shi 5 1 Department of Cardiothoracic Surgery, Shanghai University of Medicine & Health Sciences Shanghai Sixth People‘s Hospital East Campus, Shanghai, PR China 2 Department of Gastroenterology, Shanghai University of Medicine & Health Sciences Shanghai Sixth People‘s Hospital East Campus, Shanghai, PR China 3 Hangzhou Cancer Institute, Hangzhou cancer hospital, Hangzhou City, PR China 4 Department of Thoracic Surgery, Huai’an First People’s Hospital, Nanjing Medical University, Huai’an, Jiangsu, China 5 Department of Emergency, The Affiliated Huai’an Hospital of Xuzhou Medical University and The Second People’s Hospital of Huai’an, Huai’an, China * Co-first authors Correspondence to: Biao Gu, email: prof_zh@sina.com Yan Shi, email: jfmsy@163.com Keywords: lung squamous cell carcinoma, mutation, the cancer genome atlas, mRNA Received: July 04, 2016      Accepted: October 19, 2016      Published: November 07, 2016 ABSTRACT Lung squamous cell carcinoma (LUSC) is a subtype of non-small cell lung cancers which is the cause of 80% of all lung cancer deaths. The genes that highly mutated in patients with LUSC and their roles played in the tumorigenesis remains unknown. Data of patients with Lung squamous cell carcinoma (LUSC) were retrieved from The Cancer Genome Atlas (TCGA). Differentially expressed genes were identified between control and cancer samples. Patients and controls can be separated by mRNA expression level showing that the between-group variance and totally 1265 genes were differentially expressed between controls and patients. Top genes whose mutations highly occurred in patients with LUSC were identified, most of these genes were shown to be related with tumorigenesis in previous studies. All of the genes mostly mutated were independently correlated with expression levels of all genes. These mutations did not show the trend of co-occurrence. However, the influenced gene of these mutations had overlaps. After studying the intersection of these genes, a group of shared genes were identified. The shared pathways enriched which played critical role in LUSC were identified based on these shared genes. Different mutations had contribution to the progression of LUSC. Though these genes involved different specific mechanisms, most of them may share a common mechanism which is critical for LUSC. The results may suggest a neglected mechanism and also indicate a potential target for therapies.