The Methylation Analysis of KLF11 and PCDH9 Genes in Patients with Non-Small Cell Lung Cancer

Sajad Nooshin, Shohreh Zare Karizi, Morteza Karimipoor, Maryam Nooshin, Arash Matin ahmadi, Maryam Changizi maghroor, Masoumeh Masrouri

Abstract


Background: Lung cancer is the leading cause of cancer-related deaths worldwide and the 5-year survival rate is still very poor due to the lack of effective tools for early detection. Epigenetics and especially studies on DNA methylation have given important information towards a better achievement of lung cancer pathogenesis in the recent decades. The inactivation of tumor suppressor genes via promoter hypermethylation is an obvious mechanism and is straightly related to carcinogenesis. In this study, we compared the methylation status of KLF11 and PCDH9 genes in non-small cell lung cancer and adjacent normal tissues.

Methods: Genomic DNA was extracted from 30 tumor tissues, bisulfite treated and were analyzed in terms of promoter methylation status of KLF11 and PCDH9 genes by high resolution melting method. Statistical analysis was carried out by chi-square test.

Results: No significant difference in methylation level at the PCDH9 promoter region in NSCLC tumors compared with non-tumor tissues was observed (P = 0.3132, chi-square test). In contrast, the difference in methylation levels between normal and tumor tissue samples for the promoter of the KLF11 gene was quite significant (P = 0.0001).

Conclusions: Promoter methylation of KLF11 gene is an important mechanism in the development of NSCLC, therefore, it could be used as one of the potential therapeutic goals for molecular targeted therapy and epigenetic treatment. The role of the PCDH9 gene in the development of lung cancer is complex and requires more research and a larger statistical population.


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DOI: https://doi.org/10.5539/cco.v7n1p47

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Copyright (c) 2017 Sajad Nooshin, Shohreh Zare Karizi, Morteza Karimipoor

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Cancer and Clinical Oncology   ISSN 1927-4858(Print)   ISSN 1927-4866(Online)   Email: cco@ccsenet.org

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