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3. SOX17 methylation inhibits its antagonism of Wnt signaling pathway in lung cancer.

Author

Yin D, Jia Y, Yu Y, Brock MV, Herman JG, Han C, Su X, Liu Y, and Guo M

Subjects
Aged, Cell Line, Tumor, Clone Cells, Female, Gene Expression Regulation, Neoplastic, Humans, Lung Neoplasms pathology, Male, Middle Aged, SOXF Transcription Factors metabolism, Transcriptional Activation genetics, Tumor Stem Cell Assay, beta Catenin genetics, beta Catenin metabolism, DNA Methylation genetics, Lung Neoplasms genetics, SOXF Transcription Factors genetics, Wnt Signaling Pathway
Abstract

The purpose of this study was to explore epigenetic changes and functions of SOX17 in human lung cancer. Five lung cancer cell lines and 88 primary lung cancer samples were examined in this study. Methylation-specific polymerase chain reaction (MSP), semi-quantitative reverse-transcription PCR, immunohistochemistry, luciferase reporter assays, colony-formation assays, and western blotting were used to analyze methylation changes and functions of SOX17 in lung cancer. SOX17 methylation was found in 60.2% of primary human lung cancer samples, and promoter region methylation of SOX17 silenced its expression. SOX17 methylation was associated with female patients and lung cancer differentiation. Colony-formation assays revealed that SOX17 suppressed lung cancer cell proliferation. Re-expression of SOX17 inhibited Wnt signaling in H23 lung cancer cell line. SOX17 acts as a Wnt signaling inhibitor.

Published
2012

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