Evidence map›Paper›PMID 32969138›Full record

ArticleJournal of cellular and molecular medicine2020

Eva-1 homolog A promotes papillary thyroid cancer progression and epithelial-mesenchymal transition via the Hippo signalling pathway.

Bang-Yi Lin, Jia-Liang Wen, Chen Zheng, Li-Zhi Lin, Cheng-Ze Chen, Jin-Miao Qu

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

18 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Heliyon · 2024
    Article
  7. Article
  8. Article
  9. Review
  10. The Emerging Role of EVA1A in Different Types of Cancers.International journal of molecular sciences · 2022
    Review
  11. Article
  12. Article
  13. Review
  14. Frontiers in immunology · 2021
    Article
  15. Article
  16. Frontiers in immunology · 2021
    Article
  17. Article
  18. Article
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

6 authors at 1 institution in 1 country.

Bang-Yi LinDepartment of Surgical Oncology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.ORCID 0000-0001-8833-9380
Jia-Liang WenDepartment of Surgical Oncology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.ORCID 0000-0003-1493-1757
Chen ZhengDepartment of Surgical Oncology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.ORCID 0000-0002-4540-2711
Li-Zhi LinDepartment of Surgical Oncology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Cheng-Ze ChenDepartment of Surgical Oncology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.ORCID 0000-0003-2006-6915
Jin-Miao QuDepartment of Surgical Oncology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.ORCID 0000-0003-4290-7551
Wenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, the incidence of thyroid cancer is increasing worldwide. Papillary thyroid cancer (PTC) is the most common histological type of thyroid cancer. Whole-transcriptome sequence analysis was performed to further understand the primary molecular mechanisms of the occurrence and progression of PTC. Results showed that Eva-1 homolog A (EVA1A) may be a potential gene for the PTC-associated gene in thyroid cancer. In this work, the role of EVA1A expression in thyroid cancer was investigated. Real-time PCR was performed to detect the expression level of EVA1A in 43 pairs of PTC and four thyroid cancer cell lines. The Cancer Genome Atlas (TCGA) database was used to evaluate the relationship between the expression level of EVA1A and the pathological feature of PTC. The logistic regression analysis of the TCGA data set indicated that the expression of EVA1A was an independent risk factor for tumour, nde and metastasis (TNM) in PTC. This study shows the down-regulation of EVA1A inhibited the colony formation, proliferation, migration and invasion of PTC cell lines. In the protein level, knockdown of EVA1A can regulate the expression of N-cadherin, vimentin, Bcl-xL, Bax, YAP and TAZ. This study indicated that EVA1A was an oncogene associated with PTC.

Indexed as

Protein Serine-Threonine KinasesSignal TransductionAdaptor Proteins, Signal TransducingAdultAgedAntigens, CDApoptosisbcl-2-Associated X Proteinbcl-X ProteinCadherinsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticAdaptor Proteins, Signal TransducingAntigens, CDBAX protein, humanbcl-2-Associated X ProteinBCL2L1 protein, humanbcl-X ProteinCadherinsCDH2 protein, humanEVA1A protein, humanIntracellular Signaling Peptides and ProteinsMembrane ProteinsProtein Serine-Threonine KinasesTranscriptional Coactivator with PDZ-Binding Motif ProteinsTranscription FactorsVimentinVIM protein, humanWWTR1 protein, humanYAP1 protein, humanYAP-Signaling Proteinsepithelial-mesenchymal transitionEVA1AHippointrinsic apoptosis pathwaypapillary thyroid cancer

Identifiers

PMID32969138
PMCPMC7701523
OpenAlexW3088329234

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.