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The association between HPV gene expression, inflammatory agents and cellular genes involved in EMT in lung cancer tissue

Marzieh RezaeiDepartment of Biology, Science and Research Branch, Islamic Azad University, Tehran, IranShayan MostafaeiClinical Research Development Center, Imam Reza Hospital, Nurse Blvd, Kermanshah, IranAmir AghaeiDepartment of Biology, Science and Research Branch, Islamic Azad University, Tehran, IranNayyerehalsadat HosseiniMedical Genetics Research Center, Department of Medical Genetics, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, IranHassan DarabiMedical Genetics Research Center, Department of Medical Genetics, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, IranMajid NouriAJA University of Medical Sciences, Golestan Hospital Research Center, Tehran, IranAshkan EtemadiDepartment of Biology, Faculty of Science, Shahrekord University, Shahrekord, IranAndrew O’ NeillDepartment of Medicine, Trinity Centre, Tallaght University Hospital, Dublin 24, IrelandJavid Sadri NahandDepartment of Virology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, IranHamed MirzaeiBiochemistry and Nutrition Research Center, Kashan University of Medical Sciences, Kashan, IranSeamas C. DonnellyDepartment of Medicine, Trinity Centre, Tallaght University Hospital, Dublin 24, IrelandMohammad DoroudianDepartment of Cell and Molecular Biology, Faculty of Biological Sciences, Kharazmi University, Tehran, Iran. [email protected]Mohsen MoghoofeiDepartment of Microbiology, Faculty of Medicine, Kermanshah University of Medical Sciences, PO Box 6716777816, Razi Blvd, Kermanshah, Iran. [email protected]
2020en
ABI

Annotatsiya

BACKGROUND: Lung 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. METHODS: In 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. RESULTS: HPV 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. CONCLUSION: Our study suggests that HPV infection drives the induction of inflammation and EMT which may promote in the development of lung cancer.

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