Abstract
We recently reported one interesting case showing mutation-free c-KIT proto-oncogene overexpression and paradoxical hypermethylation in 54 cases of primary squamous cell carcinoma of uterine cervix (SCC). However, its molecular mechanisms still remain unknown. We propose the hypothesis that increased methylation at the CpG islands on the promoter near the first exon region might interfere with the binding of CTCF repressor with c-KIT promoter that regulates c-KIT proto-oncogene expression in such case. Further studies focusing on the status of epigenetic modifications of mutation-free c-KIT (+) tumors are encouraged.
Highlights
Epigenetic modifications may occur that result in changes in gene expression
* Correspondence: 080659@mail.fju.edu.tw; hanhaly@gmail.com †Equal contributors 5Department of Respiratory Therapy, Fu-Jen Catholic University, New Taipei, Taiwan 2Department of Pathology, Chung-Shan Medical University and Chung-Shan Medical University Hospital, Taichung, Taiwan Full list of author information is available at the end of the article uterine cervix, we recently demonstrated one case showing mutation-free, over-expression and paradoxical hypermethylation of the c-KIT proto-oncogene [4,5,6]
Our previous studies and cumulative references suggested that increased methylation at the CpG islands, which are found on the promoter near the first exon region, might interfere with the binding of CTCF repressor with c-KIT promoter that regulates c-KIT proto-oncogene expression in such a case
Summary
Epigenetic modifications may occur that result in changes in gene expression. Epigenomes represent an attractive therapeutic target. * Correspondence: 080659@mail.fju.edu.tw; hanhaly@gmail.com †Equal contributors 5Department of Respiratory Therapy, Fu-Jen Catholic University, New Taipei, Taiwan 2Department of Pathology, Chung-Shan Medical University and Chung-Shan Medical University Hospital, Taichung, Taiwan Full list of author information is available at the end of the article uterine cervix, we recently demonstrated one case showing mutation-free, over-expression and paradoxical hypermethylation of the c-KIT proto-oncogene [4,5,6].
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