Evidence map›Paper›PMID 26090866›Full record

ArticleOncotarget2015

Activation of microRNA-494-targeting Bmi1 and ADAM10 by silibinin ablates cancer stemness and predicts favourable prognostic value in head and neck squamous cell carcinomas.

Yu-Chao Chang, Chia-Ing Jan, Chih-Yu Peng, Yu-Chi Lai, Fang-Wei Hu, Cheng-Chia Yu

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
7.2field-weighted citation impact, top 2% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

  1. Pooled it
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  8. Clinico-Pathological Importance of miR-146a in Lung Cancer.Diagnostics (Basel, Switzerland) · 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

6 authors at 3 institutions in 1 country.

Yu-Chao ChangSchool of Dentistry, Chung Shan Medical University, Taichung, Taiwan.
Chia-Ing JanDepartment of Pathology, China Medical University Hospital, Taichung, Taiwan.
Chih-Yu PengSchool of Dentistry, Chung Shan Medical University, Taichung, Taiwan.
Yu-Chi LaiInstitute of Oral Sciences, Chung Shan Medical University, Taichung, Taiwan.
Fang-Wei HuSchool of Dentistry, Chung Shan Medical University, Taichung, Taiwan.
Cheng-Chia YuSchool of Dentistry, Chung Shan Medical University, Taichung, Taiwan.
Chung Shan Medical University · TWChung Shan Medical University Hospital · TWChina Medical University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor initiating cells (TICs) possessing cancer stemness were shown to be enriched after therapy, resulting in the relapse and metastasis of head and neck squamous cell carcinomas (HNC). An effective therapeutic approach suppressing the HNC-TICs would be a potential method to improve the treatments for HNC. We observed that the treatment of silibinin (SB) dose dependently down-regulated the ALDH1 activity, CD133 positivity, stemness signatures expression, self-renewal property, and chemoresistance in ALDH1+CD44+ HNC-TICs. Using miRNA-microarray and mechanistic studies, SB increased the expression of microRNA-494 (miR-494) and both Bmi1 and ADAM10 were identified as the novel targets of miR-494. Moreover, overexpression of miR-494 results in a reduction in cancer stemness. However, knockdown of miR-494 in CD44-ALDH1- non-HNC-TICs enhanced cancer stemness and oncogenicity, while co-knockdown of Bmi1 and ADAM10 effectively reversed these phenomena. Mice model showed that SB treatment by oral gavage to xenograft tumors reduced tumor growth and prolonged the survival time of tumor-bearing mice by activation of miR-494-inhibiting Bmi1/ADAM10 expression. Survival analysis indicated that a miR494highBmi1lowADAM10low phenotype predicted a favourable clinical outcome. We conclude that the inhibition of tumor aggressiveness in HNC-TICs by SB was mediated by up-regulation miR-494, suggesting that SB would be a valuable anti-cancer drug for treatment of HNC.

Indexed as

AC133 AntigenADAM10 ProteinADAM ProteinsAldehyde Dehydrogenase 1 FamilyAmyloid Precursor Protein SecretasesAnimalsAntigens, CDCarcinoma, Squamous CellCell ProliferationCell SurvivalDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionGlycoproteinsHead and Neck NeoplasmsHumansHyaluronan ReceptorsAC133 AntigenADAM10 ProteinADAM10 protein, humanADAM ProteinsAldehyde Dehydrogenase 1 FamilyALDH1A1 protein, humanALDH1A1 protein, mouseAmyloid Precursor Protein SecretasesAntigens, CDBMI1 protein, humanCD44 protein, humanGlycoproteinsHyaluronan ReceptorsIsoenzymesMembrane ProteinsMicroRNAsMIRN494 microRNA, humanPeptidesPolycomb Repressive Complex 1PROM1 protein, humanProm1 protein, mouseRetinal DehydrogenaseSilybinSilymarinhead and neck squamous cell carcinomasmicroRNA-494silibinintumor initiating cells

Identifiers

PMID26090866
PMCPMC4695166
OpenAlexW1589424230

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.