Evidence map›Paper›PMID 28515423›Full record

ArticleScientific reports2017

MiR-520b as a novel molecular target for suppressing stemness phenotype of head-neck cancer by inhibiting CD44.

Ya-Ching Lu, Ann-Joy Cheng, Li-Yu Lee, Guo-Rung You, Yan-Liang Li, Hsin-Ying Chen, Joseph T Chang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

28 citing papers in PubMed, 42 citations in OpenAlex.

  1. Differential miRNA signatures in Hepatitis E Virus Infection: Insights into acute, chronic, and pregnancy-related outcomes.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2025
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  12. A multi-omics study on cutaneous and uveal melanoma.International journal of ophthalmology · 2021
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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

7 authors at 2 institutions in 1 country.

Ya-Ching LuDepartment of Medical Biotechnology and Lab Science, College of Medicine, Chang Gung University, Taoyuan, 333, Taiwan.
Ann-Joy ChengDepartment of Medical Biotechnology and Lab Science, College of Medicine, Chang Gung University, Taoyuan, 333, Taiwan.
Li-Yu LeeDepartment of Pathology, Chang Gung Memorial Hospital - Linko, Taoyuan, 333, Taiwan.
Guo-Rung YouDepartment of Medical Biotechnology and Lab Science, College of Medicine, Chang Gung University, Taoyuan, 333, Taiwan.
Yan-Liang LiDepartment of Medical Biotechnology and Lab Science, College of Medicine, Chang Gung University, Taoyuan, 333, Taiwan.
Hsin-Ying ChenDepartment of Medical Biotechnology and Lab Science, College of Medicine, Chang Gung University, Taoyuan, 333, Taiwan.
Joseph T ChangDepartment of Radiation Oncology, Chang Gung Memorial Hospital - Linko, Taoyuan, 333, Taiwan. cgmhnog@gmail.com.
Chang Gung University · TWChang Gung Memorial Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer stem cells preferentially acquire the specific characteristics of stress tolerance and high mobility, allowing them to progress to a therapy-refractive state. To identify a critical molecule to regulate cancer stemness is indispensable to erratically cure cancer. In this study, we identified miR-520b as a novel molecular target to suppress head-neck cancer (HNC) with stemness phenotype. MiR-520b inhibited cellular migration and invasion via the mechanism of epithelial-mesenchymal transition. It also sensitized cells to therapeutic drug and irradiation. Significantly, miR-520b suppressed spheroid cell formation, as well as reduced expressions of multiple stemness regulators (Nestin, Twist, Nanog, Oct4). The CD44 molecule was identified as a direct target of miR-520b, as shown by the reverse correlative expressions, the response to miR-520 modulation, the luciferase reporter assay, and the functional rescue analyses. These cellular results were confirmed by a tumor xenograft mice study. Administration of miR-520b dramatically restrained tumorigenesis and liver colonization. Conversely, miR-520b silencing led to an acceleration of tumor growth. Taken together, our study demonstrated that miR-520b inhibits the malignancy of HNC through regulation of cancer stemness conversion by targeting CD44. MiR-520b may serve as an emerging therapeutic target that may be further developed for the intervention of refractory HNC.

Indexed as

Gene Expression Regulation, NeoplasticRNA InterferenceAnimalsAntineoplastic AgentsCell Line, TumorCell MovementCell ProliferationCell Self RenewalCell Transformation, NeoplasticEpithelial-Mesenchymal TransitionHead and Neck NeoplasmsHumansHyaluronan ReceptorsMiceMicroRNAsMultigene FamilyAntineoplastic AgentsCD44 protein, humanHyaluronan ReceptorsMicroRNAsMIRN520 microRNA, human

Identifiers

PMID28515423
PMCPMC5435724
OpenAlexW2612463309

What OpenQuestion holds

Textmetadata
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.