Abstract

BackgroundLung cancer is a leading cause of cancer morbidity and mortality worldwide. Several studies have suggested that Human papillomavirus (HPV) infection is an important risk factor in the development of lung cancer. In this study, we aim to address the role of HPV in the development of lung cancer mechanistically by examining the induction of inflammation and epithelial-mesenchymal transition (EMT) by this virus.MethodsIn this case-control study, tissue samples were collected from 102 cases with lung cancer and 48 controls. We examined the presence of HPV DNA and also the viral genotype in positive samples. We also examined the expression of viral genes (E2, E6 and E7), anti-carcinogenic genes (p53, retinoblastoma (RB)), and inflammatory cytokines in HPV positive cases.ResultsHPV DNA was detected in 52.9% (54/102) of the case samples and in 25% (12/48) of controls. A significant association was observed between a HPV positive status and lung cancer (OR = 3.37, 95% C.I = 1.58–7.22, P = 0.001). The most prevalent virus genotype in the patients was type 16 (38.8%). The expression of p53 and RB were decreased while and inflammatory cytokines were increased in HPV-positive lung cancer and HPV-positive control tissues compared to HPV-negative lung cancer and HPV-negative control tissues. Also, the expression level of E-cad and PTPN-13 genes were decreased in HPV- positive samples while the expression level of SLUG, TWIST and N-cad was increased in HPV-positive samples compared to negative samples.ConclusionOur study suggests that HPV infection drives the induction of inflammation and EMT which may promote in the development of lung cancer.

Highlights

  • Lung cancer is a leading cause of cancer morbidity and mortality worldwide

  • Human papillomavirus (HPV) DNA was detected in 52.9% of the lung cancer specimens and in 25% of control samples

  • We examined the potential role of HPV in lung cancer pathogenesis in two ways: i) the impact of HPV on the expression of genes involved in epithelial-mesenchymal transition (EMT), ii) the impact of HPV in the development of chronic inflammation and microenvironment alteration

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Summary

Introduction

Several studies have suggested that Human papillomavirus (HPV) infection is an important risk factor in the development of lung cancer. We aim to address the role of HPV in the development of lung cancer mechanistically by examining the induction of inflammation and epithelial-mesenchymal transition (EMT) by this virus. There are several types of primary lung cancer which, are divided into two main groups; small cell lung cancer (SCLC) and nonsmall cell lung cancer (NSCLC). NSCLC are divided into three common types; squamous cell carcinoma, large cell carcinoma and adenocarcinoma [2]. Numerous infectious agents have been shown to be involved in a myriad of lung diseases including cancer, Idiopathic Pulmonary Fibrosis (IPF) and Chronic Obstructive Pulmonary Disease (COPD) [8,9,10]

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