Evidence map›Paper›PMID 34462424›Full record

ArticleCell death discovery2021

Loss of ID3 drives papillary thyroid cancer metastasis by targeting E47-mediated epithelial to mesenchymal transition.

Sunwang Xu, Caiqin Mo, Junyu Lin, Yixing Yan, Xiaoyu Liu, Kunlin Wu, Huihao Zhang, Youzhi Zhu, Ling Chen, Xiangjin Chen

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

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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

10 authors at 1 institution in 1 country.

Sunwang Xu *Department of Thyroid and Breast Surgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China. xusw1206@163.com.ORCID http://orcid.org/0000-0001-5588-3777
Caiqin Mo *Department of Thyroid and Breast Surgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China.
Junyu Lin *Department of Thyroid and Breast Surgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China.
Yixing YanDepartment of Thyroid and Breast Surgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China.
Xiaoyu LiuDepartment of Thyroid and Breast Surgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China.
Kunlin WuDepartment of Thyroid and Breast Surgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China.
Huihao ZhangDepartment of Thyroid and Breast Surgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China.
Youzhi ZhuDepartment of Thyroid and Breast Surgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China.
Ling ChenDepartment of Thyroid and Breast Surgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China. alichoo@163.com.ORCID http://orcid.org/0000-0002-4607-617X
Xiangjin ChenDepartment of Thyroid and Breast Surgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China. rjbhcxj@fjmu.edu.cn.ORCID http://orcid.org/0000-0002-0132-6673
Fujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Papillary thyroid cancer (PTC) is the main histological type of thyroid cancer and accounts for almost all increased cases worldwide. Patients with PTC exhibit a favorable prognosis, but the fact that PTC is often accompanied by a high prevalence of lymph node metastasis (LNM) means that the overall recurrence-free survival rate in PTC patients is relatively low. Herein, we identified that ID3 expression is subdued in PTC tissues and closely associated with LNM and a poor disease-free survival outcome in PTC patients. The main contributor to this gene repression is the hypermethylation of the CpG island at the promoter of ID3. Besides, we uncovered that a loss of ID3 promotes invasion and migration of PTC cells, while an ectopic overexpression of ID3 inhibits invasion and migration. Mechanistically, ID3 exhibits tumor suppressor functions in PTC cells by interacting with E47 to form heterodimers that prevent E47 binding to CDH1 promoter and maintaining CDH1 transcription and epithelial phenotype in PTC cells. Taken together, our study demonstrates that ID3 plays a tumor suppressor role in PTC and impedes metastasis by inhibiting E47-mediated epithelial to mesenchymal transition.

Identifiers

PMID34462424
PMCPMC8405699
OpenAlexW3196471147

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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.