Evidence map›Paper›PMID 32046777›Full record

ArticleClinical epigenetics2020

Methylation silencing of TGF-β receptor type II is involved in malignant transformation of esophageal squamous cell carcinoma.

Yarui Ma, Siyuan He, Aiai Gao, Ying Zhang, Qing Zhu, Pei Wang, Beibei Yang, Huihui Yin, Yifei Li, Jinge Song and 7 more

Open access · goldAbstract read
In one paragraph

Article in Clinical epigenetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. RBM15 increase tumor-infiltrating CD4+ T cell in ESCCAmerican journal of cancer research · 2024
    Article
  6. Article
  7. miR-17-5p slows progression of hepatocellular carcinoma by downregulating TGFβR2.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Article
  8. Article
  9. Review
  10. Article
  11. Clinical utility ofArchives of endocrinology and metabolism · 2021
    Article
  12. Identification of a DNA Methylation-Based Prognostic Signature for Patients with Triple-Negative Breast Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2021
    Article
  13. Crosstalk Between Inflammatory Signaling and Methylation in Cancer.Frontiers in cell and developmental biology · 2021
    Review
  14. Article
  15. Review
  16. Observational
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 3 institutions in 2 countries.

Yarui MaState Key Lab of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Research Building, No.17 Panjiayuan Nanli, Chaoyang District, Beijing, 100021, China.
Siyuan HeState Key Lab of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Research Building, No.17 Panjiayuan Nanli, Chaoyang District, Beijing, 100021, China.
Aiai GaoDepartment of Gastroenterology & Hepatology, Chinese PLA General Hospital, Research Building, No.28 Fuxing Road, Haidian District, Beijing, 100853, China.
Ying ZhangState Key Lab of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Research Building, No.17 Panjiayuan Nanli, Chaoyang District, Beijing, 100021, China.
Qing ZhuState Key Lab of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Research Building, No.17 Panjiayuan Nanli, Chaoyang District, Beijing, 100021, China.
Pei WangState Key Lab of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Research Building, No.17 Panjiayuan Nanli, Chaoyang District, Beijing, 100021, China.
Beibei YangState Key Lab of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Research Building, No.17 Panjiayuan Nanli, Chaoyang District, Beijing, 100021, China.
Huihui YinState Key Lab of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Research Building, No.17 Panjiayuan Nanli, Chaoyang District, Beijing, 100021, China.
Yifei LiState Key Lab of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Research Building, No.17 Panjiayuan Nanli, Chaoyang District, Beijing, 100021, China.
Jinge SongState Key Lab of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Research Building, No.17 Panjiayuan Nanli, Chaoyang District, Beijing, 100021, China.
Pinli YueState Key Lab of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Research Building, No.17 Panjiayuan Nanli, Chaoyang District, Beijing, 100021, China.
Mo LiState Key Lab of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Research Building, No.17 Panjiayuan Nanli, Chaoyang District, Beijing, 100021, China.
Dandan ZhangMOE Key Laboratory of Metabolism and Molecular Medicine, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences and Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Yun LiuMOE Key Laboratory of Metabolism and Molecular Medicine, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences and Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Xiaobing WangState Key Lab of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Research Building, No.17 Panjiayuan Nanli, Chaoyang District, Beijing, 100021, China. wangxb@cicams.ac.cn.ORCID 0000-0002-0907-364X
Mingzhou GuoDepartment of Gastroenterology & Hepatology, Chinese PLA General Hospital, Research Building, No.28 Fuxing Road, Haidian District, Beijing, 100853, China. mzguo@hotmail.com.
Yuchen JiaoState Key Lab of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Research Building, No.17 Panjiayuan Nanli, Chaoyang District, Beijing, 100021, China. Jiaoyuchen@cicams.ac.cn.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNChinese PLA General Hospital · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlthough massive studies have been conducted to investigate the mechanisms of esophageal squamous cell carcinoma (ESCC) carcinogenesis, the understanding of molecular alterations during the malignant transformation of epithelial dysplasia is still lacking, especially regarding epigenetic changes.

resultsTo better characterize the methylation changes during the malignant transformation of epithelial dysplasia, a whole-genome bisulfite sequencing analysis was performed on a series of tumor, dysplastic, and non-neoplastic epithelial tissue samples from esophageal squamous cell carcinoma (ESCC) patients. Promoter hypermethylation in TGF-β receptor type II (TGFBR2), an important mediator of TGF-β signaling, was identified. Further, we evaluated the methylation and expression of TGFBR2 in tumor samples through The Cancer Genome Atlas multiplatform data as well as immunohistochemistry. Moreover, treatment of ESCC cell lines with5-Aza-2'-deoxycytidine, a DNA methyltransferase inhibitor, reactivated the expression of TGFBR2. The lentiviral mediating the overexpression of TGFBR2 inhibited the proliferation of ESCC cell line by inducing cell cycle G2/M arrest. Furthermore, the overexpression of TGFBR2 inhibited the tumor growth obviously in vivo.

conclusionsThe characterization of methylation silencing of TGFBR2 in ESCC will enable us to further explore whether this epigenetic change could be considered as a predictor of malignant transformation in esophageal epithelial dysplasia and whether use of a TGFBR2 agonist may lead to a new therapeutic strategy in patients with ESCC.

Indexed as

AnimalsCarcinogenesisDecitabineDNA MethylationDown-RegulationEnzyme InhibitorsEpigenesis, GeneticEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaExome SequencingFemaleG2 Phase Cell Cycle CheckpointsGene SilencingHeterograftsHumansMiceDecitabineEnzyme InhibitorsReceptor, Transforming Growth Factor-beta Type IITGFBR2 protein, humanCancer diagnosisEsophageal squamous cell carcinomaMethylation changesTGFBR2TreatmentWhole genome bisulfite sequencing

Identifiers

PMID32046777
PMCPMC7014638
OpenAlexW3008298509

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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.