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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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Published in: | Journal of Cancer 2021-01, Vol.12 (6), p.1634-1643 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that cite this one |
Online Access: | Get full text |
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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 |
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ISSN: | 1837-9664 1837-9664 |
DOI: | 10.7150/jca.49231 |