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The Study on the Expression of ADAM23 and Its Correlation with Promoter Methylation in Non-small Cell Lung Carcinoma

Author: HuChunYan
Tutor: ZhouJianHua
School: Central South University
Course: Pathology and Pathophysiology
Keywords: Methylation-specific polymerase chain reaction (MSP) Disintegrin - metalloproteinase 23 ανβ3 Non - small cell lung cancer 5 - aza -2'- deoxycytidine ( 5 -Aza -2' -dC )
CLC: R734.2
Type: Master's thesis
Year: 2011
Downloads: 28
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Abstract


Lung cancer is one of the most common malignant tumor. Intracellular oncogene activation and / or inactivation of tumor suppressor genes is a major cause of lung cancer occurred. Recent studies have shown that epigenetic changes play an important role in the occurrence and development of lung cancer, including DNA methylation abnormalities caused by the tumor suppressor gene silencing plays a key role in tumor development. Therefore, the study of new tumor suppressor gene dysfunction and its mechanism in lung cancer, is of great significance in elucidating the pathogenesis of lung cancer, and to guide clinical treatment. Disintegrin - metalloproteinase 23 (ADisintegrin And Metalloprotease23, ??ADAM23) gene belongs to the ADAM family members, is a transmembrane glycoprotein mediated cell asked cell - matrix adhesion between fusion, in the process of tumor invasion and metastasis specific activation of integrin receptors avβ3, thereby promoting tumor angiogenesis, and accelerated tumor cell growth and migration. Recent studies have reported that ADAM23 as a tumor suppressor gene and its expression in the absence of breast cancer, gastric cancer, pancreatic cancer, laryngeal cancer, colorectal cancer [3-7] closely related to the occurrence and development of malignant tumors, and the mechanism of the gene start CpG island methylation abnormalities are highly correlated. However, ADAM23 expression in non-small cell lung cancer (non-small cell lung cancer, NSCLC) and its promoter methylation modification, and role in the development of lung cancer, at home and abroad have no relevant reports. In this study, through the analysis of ADAM23 expression in non-small cell lung cancer and to reveal the role of ADAM23 in non-small cell lung development, and analysis of its promoter methylation status reveals the mechanism of its downregulation of lung cancer the treatment and prognosis of new targets. Objective: To detect ADAM23 avβ3 expression in non-small cell lung cancer and its relationship with clinical and pathological features of patients; analysis of the relationship of the ADAM23 gene promoter region CpG island methylation and its expression reveal ADAM23 in non-small cell lung cancer 's role is to provide a theoretical basis and experimental evidence. Methods: (1) application of immunohistochemical techniques and RT-PCR method detected 52 cases of non-small cell lung cancer and its paired adjacent organizations and 8 benign lesions of ADAM23, avβ3 in the expression, analysis of its correlation with the clinical and pathological features . By Western blotting and RT-PCR method to detect ADAM23 in lung squamous cell carcinoma cells (SK-MES-1) and lung adenocarcinoma cells (A549, SPC-A1, LTEP-a-2) expression. (2) application of the methylation-specific PCR (MSP) were detected in fresh tissue and cells ADAM23 gene promoter methylation analysis of its correlation with expression. (3) Application demethylation specific drugs 5 - aza-2'-deoxycytidine (5-Aza-2'-dC) to deal with non-small cell lung cancer cells detected before and after drug treatment ADAM23 gene expression and promoter the methylation change the situation. Results: (1) the ADAM23 protein positive rate in the non-small cell lung cancer (38.5%) than in adjacent tissues (86.5%) and pulmonary benign lesions (87.5%) (P lt; O.05), while αvβ3 protein The positive rate (80.8%) was higher than the adjacent tissues (26.9%) and pulmonary benign lesions (37.5%) (P

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