Evidence map›Paper›PMID 32752071›Full record

ArticleInternational journal of molecular sciences2020

Role of miR-96/EVI1/miR-449a Axis in the Nasopharyngeal Carcinoma Cell Migration and Tumor Sphere Formation.

Lai-Sheung Chan, Hong-Lok Lung, Roger Kai-Cheong Ngan, Anne Wing-Mui Lee, Sai Wah Tsao, Kwok-Wai Lo, Michael Kahn, Maria Li Lung, Rotraud Wieser, Nai-Ki Mak

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 38% 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

7 citing papers in PubMed, 10 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 6 institutions in 4 countries.

Lai-Sheung ChanDepartment of Biology, Hong Kong Baptist University, Kowloon Tong, Hong Kong, China.
Hong-Lok LungDepartment of Chemistry, Hong Kong Baptist University, Kowloon Tong, Hong Kong, China.
Roger Kai-Cheong NganDepartment of Clinical Oncology, University of Hong Kong, Pokfulam, Hong Kong, China.
Anne Wing-Mui LeeDepartment of Clinical Oncology, University of Hong Kong, Pokfulam, Hong Kong, China.ORCID 0000-0003-2972-0231
Sai Wah TsaoCenter for Nasopharyngeal Carcinoma Research, University of Hong Kong, Pokfulam, Hong Kong, China.
Kwok-Wai LoDepartment of Anatomical and Cellular Pathology and State Key Laboratory in Oncology in South China, The Chinese University of Hong Kong, Central Ave, Hong Kong, China.
Michael KahnDepartment of Molecular Medicine, Beckman Research Institute at City of Hope, Duarte, CA 91010-3000, USA.
Maria Li LungDepartment of Clinical Oncology, University of Hong Kong, Pokfulam, Hong Kong, China.ORCID 0000-0003-2559-3626
Rotraud WieserDivision of Oncology, Department of Medicine I, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0003-4384-6658
Nai-Ki MakDepartment of Biology, Hong Kong Baptist University, Kowloon Tong, Hong Kong, China.ORCID 0000-0001-9563-5372
Hong Kong Baptist University · HKQueen Mary Hospital · CNChinese University of Hong Kong · HKCity of Hope · USMedical University of Vienna · ATUniversity of Hong Kong · HK

Funding

Hong Kong Baptist University HKBU SDF 15-1012-P04NIH HHS P30CA014089, R01CA166161, R21NS074392, R21AI105057, and R01HL112638.Research Grants Council, University Grants Committee AoE/M 06/08
6 · The paper itself

Abstract

The Wnt signaling pathway is one of the major signaling pathways used by cancer stem cells (CSC). Ecotropic Viral Integration Site 1 (EVI1) has recently been shown to regulate oncogenic development of tumor cells by interacting with multiple signaling pathways, including the Wnt signaling. In the present study, we found that the Wnt modulator ICG-001 could inhibit the expression of EVI1 in nasopharyngeal carcinoma (NPC) cells. Results from loss-of-function and gain-of-function studies revealed that EVI1 expression positively regulated both NPC cell migration and growth of CSC-enriched tumor spheres. Subsequent studies indicated ICG-001 inhibited EVI1 expression via upregulated expression of miR-96. Results from EVI1 3'UTR luciferase reporter assay confirmed that EVI1 is a direct target of miR-96. Further mechanistic studies revealed that ICG-001, overexpression of miR-96, or knockdown of EVI1 expression could restore the expression of miR-449a. The suppressive effect of miR-449a on the cell migration and tumor sphere formation was confirmed in NPC cells. Taken together, the miR-96/EVI1/miR-449a axis is a novel pathway involved in ICG-001-mediated inhibition of NPC cell migration and growth of the tumor spheres.

Indexed as

3' Untranslated RegionsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansMDS1 and EVI1 Complex Locus ProteinMicroRNAsNasopharyngeal CarcinomaNeoplastic Stem CellsWnt Signaling Pathway3' Untranslated RegionsMDS1 and EVI1 Complex Locus ProteinMECOM protein, humanMicroRNAsMIRN449 microRNA, humanMIRN96 microRNA, humanEVI1ICG-001miR-449amiR-96nasopharyngeal carcinoma

Identifiers

PMID32752071
PMCPMC7432346
OpenAlexW3046559181

What OpenQuestion holds

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LicenceCC BY
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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.