Methylomic analysis identifies C11orf87 as a novel epigenetic biomarker for GI cancers

doi:10.1371/journal.pone.0250499

中山醫學大學機構典藏 CSMUIR > 中山醫學大學研究成果 > 期刊論文 > Item 310902500/23507

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/23507

Title:	Methylomic analysis identifies C11orf87 as a novel epigenetic biomarker for GI cancers
Authors:	Tran, MTMT;Yeh, KT;Chuang, YM;Hsu, PY;Low, JT;Kumari, H;Lee, YT;Chen, YC;Huang, WH;Jin, HC;Lin, SH;Chan, MWY
Date:	2021
Issue Date:	2022-08-05T09:38:24Z (UTC)
Publisher:	PUBLIC LIBRARY SCIENCE
ISSN:	1932-6203
Abstract:	Gastric cancer is one of the leading causes of cancer death worldwide. Previous studies demonstrated that activation of STAT3 is crucial for the development and progression of gastric cancer. However, the role of STAT3 in neuronal related gene methylation in gastric cancer has never been explored. In this study, by using DNA methylation microarray, we identified a potential STAT3 target, C11orf87, showing promoter hypomethylation in gastric cancer patients with lower STAT3 activation and AGS gastric cancer cell lines depleted with STAT3 activation. Although C11orf87 methylation is independent of its expression, ectopic expression of a constitutive activated STAT3 mutant upregulated its expression in gastric cancer cell line. Further bisulfite pyrosequencing demonstrated a progressive increase in DNA methylation of this target in patient tissues from gastritis, intestinal metaplasia, to gastric cancer. Intriguingly, patients with higher C11orf87 methylation was associated with better survival. Furthermore, hypermethylation of C11orf87 was also frequently observed in other GI cancers, as compared to their adjacent normal tissues. These results suggested that C11orf87 methylation may serve as a biomarker for diagnosis and prognosis of GI cancers, including gastric cancer. We further postulated that constitutive activation of STAT3 might be able to epigenetically silence C11orf87 as a possible negative feedback mechanism to protect the cells from the overactivation of STAT3. Targeted inhibition of STAT3 may not be appropriate in gastric cancer patients with promoter hypermethylation of C11orf87.
URI:	http://dx.doi.org/10.1371/journal.pone.0250499 https://www.webofscience.com/wos/woscc/full-record/WOS:000644138300138 https://ir.csmu.edu.tw:8080/handle/310902500/23507
Relation:	PLOS ONE ,2021,v16,issue 4
Appears in Collections:	[中山醫學大學研究成果] 期刊論文

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