Evidence map›Paper›PMID 28703658›Full record

ArticleEpigenetics2017

Epigenetic silencing of miR-203 in Kazakh patients with esophageal squamous cell carcinoma by MassARRAY spectrometry.

Xiaobin Cui, Xi Chen, Weiwei Wang, Aimin Chang, Lan Yang, Chunxia Liu, Hao Peng, Yutao Wei, Weihua Liang, Shugang Li and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Epigenetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. The Association of Methylation Level in thePharmacogenomics and personalized medicine · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors at 4 institutions in 1 country.

Xiaobin Cuia Department of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases , Shihezi University School of Medicine , Shihezi , China.
Xi Chena Department of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases , Shihezi University School of Medicine , Shihezi , China.
Weiwei Wangc Department of Pathology , Zhucheng Maternal and Child Care Service Centre , Weifang , China.
Aimin Changd Department of Pathology , People's Hospital of Wusu , Tacheng , China.
Lan Yanga Department of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases , Shihezi University School of Medicine , Shihezi , China.
Chunxia Liua Department of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases , Shihezi University School of Medicine , Shihezi , China.
Hao Penga Department of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases , Shihezi University School of Medicine , Shihezi , China.
Yutao Weie Department of Thoracic and Cardiovascular Surgery , The First Affiliated Hospital, Shihezi University School of Medicine , Shihezi , China.
Weihua Lianga Department of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases , Shihezi University School of Medicine , Shihezi , China.
Shugang Lia Department of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases , Shihezi University School of Medicine , Shihezi , China.
Ning Wanga Department of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases , Shihezi University School of Medicine , Shihezi , China.
Wei Liua Department of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases , Shihezi University School of Medicine , Shihezi , China.
Jianming Hua Department of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases , Shihezi University School of Medicine , Shihezi , China.
Wenjie Zhanga Department of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases , Shihezi University School of Medicine , Shihezi , China.
Lidong Wangf Henan Key Laboratory for Esophageal Cancer Research , Department of Basic Oncology and Pathology at College of Medicine , The First and The Second Affiliated Hospital, Zhengzhou University , Zhengzhou , Henan , China.
Yunzhao Chena Department of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases , Shihezi University School of Medicine , Shihezi , China.
Feng Lia Department of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases , Shihezi University School of Medicine , Shihezi , China.
Shihezi University · CNWeifang Maternity and Child Care Hospital · CNZhengzhou University · CNZoucheng People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulation of miR-203 by promoter methylation is associated with the development of various cancers. We aimed to explore the underlying link between promoter methylation and miR-203 expression in Kazakh esophageal squamous cell carcinoma (ESCC). MassARRAY® System spectrometry was used to quantitatively analyze the DNA methylation of 32 CpG sites within miR-203 in 99 Kazakh ESCC and 46 normal esophageal tissues (NETs) with similar population characteristics. We conducted real-time PCR to detect miR-203 expression levels and evaluated their association with methylation. Eleven CpG units within miR-203 promoter were frequently hypermethylated in ESCC compared with NETs (P < 0.05). The hypermethylation of several CpG units positively correlated with age, lower esophagus, constrictive type of ESCC, and moderately differentiated ESCC. Given the involvement of human papillomavirus (HPV) in etiology of ESCC was confirmed from our previous reports, herein we found that CpG units within miR-203 in HPV16-positive ESCC are more heavily methylated. Furthermore, miR-203 expression showed a nearly 4.5-fold decrease in ESCC than NETs (0.206 ± 0.336 vs. 0.908 ± 1.424, P < 0.001) and was significantly associated with lymph node metastasis (P = 0.012). The expression of miR-203 with 11 completely hypermethylated CpG units was approximately 6.5-fold lower than that with at least 1 unmethylated CpG unit (P < 0.001) and especially the CpG_15.16 and CpG_31.32 with higher methylation levels in ESCC tissues exhibited lower expression levels of miR-203, which indicated a reverse association between miR-203 methylation and expression. Hypermethylated miR-203 is a potential biomarker and targeted delivery of miR-203 could therefore serve as a preventive or therapeutic strategy for Kazakh ESCC.

Indexed as

DNA MethylationGene SilencingAgedAsian PeopleCarcinoma, Squamous CellCpG IslandsEsophageal NeoplasmsFemaleHumansMaleMicroRNAsMiddle AgedMicroRNAsMIRN203 microRNA, humanEsophageal squamous cell carcinomaKazakhmethylationmiR-203

Identifiers

PMID28703658
PMCPMC5687329
OpenAlexW2736078726

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.