Evidence map›Paper›PMID 32037949›Full record

ArticleCancer biology & therapy2020

The stress-activated protein kinase pathway and the expression of stanniocalcin-1 are regulated by miR-146b-5p in papillary thyroid carcinogenesis.

Abeer Al-Abdallah, Iman Jahanbani, Heba Mehdawi, Rola H Ali, Nabeel Al-Brahim, Olusegun Mojiminiyi

Open access · bronzeAbstract read
In one paragraph

Article in Cancer biology & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Article
  3. MiR-501-3p/SPC24 axis affects cell proliferation, migration, invasion, apoptosis, and prognosis in renal cell carcinoma.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2025
    Article
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  5. Review
  6. Article
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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

6 authors at 2 institutions in 1 country.

Abeer Al-AbdallahPathology Department, Kuwait University, Kuwait City, Kuwait.ORCID 0000-0001-8577-802X
Iman JahanbaniPathology Department, Kuwait University, Kuwait City, Kuwait.
Heba MehdawiPathology Department, Kuwait University, Kuwait City, Kuwait.
Rola H AliPathology Department, Kuwait University, Kuwait City, Kuwait.
Nabeel Al-BrahimPathology Department, Farwaniya Hospital, Kuwait City, Kuwait.
Olusegun MojiminiyiPathology Department, Kuwait University, Kuwait City, Kuwait.
Kuwait University · KWFarwaniya Hospital · KW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Papillary thyroid cancer (PTC) is the most common type of thyroid cancer. Deciphering the pathophysiological mechanisms that contribute to PTC development is essential to the discovery of optimal diagnostic and therapeutic approaches. MiR-146b-5p has been identified as a cancer-associated microRNA highly up-regulated in PTC. This study explores the hypothesis that miR-146b-5p contributes to papillary thyroid carcinogenesis through regulation of cell signaling pathways in a manner that overcomes the cellular growth suppressive events and provides survival advantage. The effect of miR-146b-5p inhibition on major cancer related signaling pathways and expression of Stanniocalcin-1 (STC1), an emerging molecule associated with stress response and carcinogenesis, was tested in cultured primary thyroid cells using luciferase reporter assays, quantitative real-time PCR, immunofluorescence staining, and flow cytometry. Our results demonstrated that miR-146b-5p inhibits the JNK/AP1 pathway activity and down-regulates the expression of STC-1 in thyroid-cultured cells and in thyroid tissue samples. In the presence of miR-146b-5p, PTC cells were resistant to cell death in response to oxidative stress. This is a novel report that miR-146b-5p directly targets STC1 and regulates the activity of JNK/AP1 pathway. Considering the importance of the JNK/AP1 pathway and STC1 in mediating many physiological and pathological processes like apoptosis, stress response and cellular metabolism, a biological regulator of these pathways would have a great scientific and clinical significance.

Indexed as

Gene Expression Regulation, NeoplasticOxidative StressCarcinogenesisCell MovementCell ProliferationGlycoproteinsHumansMicroRNAsMitogen-Activated Protein Kinase 8Thyroid Cancer, PapillaryThyroid NeoplasmsTumor Cells, CulturedGlycoproteinsMicroRNAsMIRN146 microRNA, humanMitogen-Activated Protein Kinase 8teleocalcinactivator protein-1miRNA, papillary thyroid carcinomastanniocalcin-1stress-activated protein kinase

Identifiers

PMID32037949
PMCPMC7515490
OpenAlexW3006082333

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.