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DNA methylation integratedly modulates the expression of Pit-Oct-Unt transcription factors in esophageal squamous cell carcinoma

Dysregulation of Pit-Oct-Unc family transcription factors has been implicated in esophageal squamous cell carcinoma (ESCC). In this study, we evaluated the expression and promoter methylation status of Octamer (OCT) transcription factor genes in human ESCC clinical specimens to investigate the mecha...

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Bibliographic Details
Published in:Journal of Cancer 2021-01, Vol.12 (6), p.1634-1643
Main Authors: He, Wei, Gong, Shuai, Wang, Xin, Dong, Xinhua, Cheng, Hua
Format: Article
Language:English
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Summary:Dysregulation of Pit-Oct-Unc family transcription factors has been implicated in esophageal squamous cell carcinoma (ESCC). In this study, we evaluated the expression and promoter methylation status of Octamer (OCT) transcription factor genes in human ESCC clinical specimens to investigate the mechanism underlying this observation along with the clinical significance. Total DNA or RNA was extracted from ESCC tissue specimens and the mRNA level of genes encoding the transcription factors OCT1, OCT2, OCT3/OCT4, OCT5, OCT7, OCT9, and OCT11 were evaluated by quantitative PCR. The DNA methylation status of gene promoters was assessed by bisulfite pyrosequencing and next-generation sequencing. The relationship between the expression of these transcription factors and ESCC proliferation was investigated and with the colony formation assay and a mouse xenograft tumor model, respectively. We also examined the correlation between gene expression and promoter methylation and clinicopathologic characteristics of ESCC. was upregulated whereas , , and were downregulated in ESCC compared to non-tumor tissue. , , and were undetected in all samples. , , and levels were negatively correlated with the methylation of their respective promoters, but there was no relationship between expression and promoter methylation status. Changes in promoter methylation rate underlie the observed alterations in , , and expression in ESCC, whereas another mechanism is likely responsible for the dysregulation of
ISSN:1837-9664
1837-9664
DOI:10.7150/jca.49231