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TET1介导的DNA低甲基化调控肺癌中MUC4的表达。

TET1-mediated DNA hypomethylation regulates the expression of MUC4 in lung cancer.

作者信息

Yokoyama Seiya, Higashi Michiyo, Tsutsumida Hideaki, Wakimoto Jouji, Hamada Tomofumi, Wiest Edwin, Matsuo Kei, Kitazono Ikumi, Goto Yuko, Guo Xin, Hamada Taiji, Yamada Sohsuke, Hiraki Tsubasa, Yonezawa Suguru, Batra Surinder K, Hollingsworth Michael A, Tanimoto Akihide

机构信息

Department of Pathology, Research Field in Medicine and Health Sciences, Medical and Dental Sciences Area, Research and Education Assembly, Kagoshima University, Sakuragoaka, Japan.

Center for the Research of Advanced Diagnosis and Therapy of Cancer, Graduate School of Medical and Dental Sciences, Kagoshima University, Japan.

出版信息

Genes Cancer. 2017 Mar;8(3-4):517-527. doi: 10.18632/genesandcancer.139.

DOI:10.18632/genesandcancer.139
PMID:28680536
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5489649/
Abstract

Lung cancer remains a disease of high mortality, despite advanced diagnostic techniques. Mucins (MUC) play crucial roles in carcinogenesis and tumor invasion in lung neoplasms. Our immunohistochemistry (IHC) studies have shown that high MUC4 expression correlates with a poor outcome. We have also shown that the expression of several mucin genes in cancer cell lines is regulated by DNA methylation. We evaluated the expression level of MUC4, mRNA and several DNA hypomethylation factors in lung tissue samples from 33 patients with various lung lesions. The results indicated that the DNA methylation status of matched the expression level of mRNA. In addition, the (Ten-Eleven Translocation) mRNA showed a significant correlation with the status of DNA methylation of . Furthermore, the treatment of a lung cancer cell line with siRNA caused a reduction in mRNA expression. Thus, we suggest that mediated DNA hypomethylation plays a key role in the expression of MUC4. This is the first report that TET1 mediated DNA hypomethylation regulates the expression of MUC4 in lung cancer. The analysis of these epigenetic changes may be useful for diagnosing carcinogenic risk.

摘要

尽管诊断技术不断进步，但肺癌仍然是一种高死亡率的疾病。粘蛋白（MUC）在肺癌的致癌作用和肿瘤侵袭中起着关键作用。我们的免疫组织化学（IHC）研究表明，MUC4高表达与不良预后相关。我们还表明，癌细胞系中几种粘蛋白基因的表达受DNA甲基化调控。我们评估了33例患有各种肺部病变患者的肺组织样本中MUC4、mRNA和几种DNA低甲基化因子的表达水平。结果表明，DNA甲基化状态与mRNA表达水平相匹配。此外，TET（十一 - 易位）mRNA与MUC4的DNA甲基化状态显示出显著相关性。此外，用TET1 siRNA处理肺癌细胞系导致MUC4 mRNA表达降低。因此，我们认为TET1介导的DNA低甲基化在MUC4的表达中起关键作用。这是第一份关于TET1介导的DNA低甲基化调节肺癌中MUC4表达的报告。对这些表观遗传变化的分析可能有助于诊断致癌风险。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3ec/5489649/f5147cb3f2c6/ganc-08-517-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3ec/5489649/111a68142dcd/ganc-08-517-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3ec/5489649/ea4d120ab4df/ganc-08-517-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3ec/5489649/3a98ceecc556/ganc-08-517-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3ec/5489649/f5147cb3f2c6/ganc-08-517-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3ec/5489649/111a68142dcd/ganc-08-517-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3ec/5489649/ea4d120ab4df/ganc-08-517-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3ec/5489649/3a98ceecc556/ganc-08-517-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3ec/5489649/f5147cb3f2c6/ganc-08-517-g004.jpg

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