Evidence map›Paper›PMID 27521216›Full record

ArticleOncotarget2016

CD44 and CD24 coordinate the reprogramming of nasopharyngeal carcinoma cells towards a cancer stem cell phenotype through STAT3 activation.

Yao-An Shen, Chia-Yu Wang, Hui-Yen Chuang, John Jeng-Jong Hwang, Wei-Hsin Chi, Chih-Hung Shu, Ching-Yin Ho, Wing-Yin Li, Yann-Jang Chen

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.2field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
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  5. The Hyaluronan/CD44 Axis: A Double-Edged Sword in Cancer.International journal of molecular sciences · 2023
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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

9 authors at 3 institutions in 1 country.

Yao-An ShenInstitute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei 112, Taiwan.
Chia-Yu WangDepartment of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei 112, Taiwan.
Hui-Yen ChuangDepartment of Biomedical Imaging and Radiological Sciences, National Yang-Ming University, Taipei 112, Taiwan.
John Jeng-Jong HwangDepartment of Biomedical Imaging and Radiological Sciences, National Yang-Ming University, Taipei 112, Taiwan.
Wei-Hsin ChiDepartment of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei 112, Taiwan.
Chih-Hung ShuDepartment of Otorhinolaryngology, Taipei Veterans General Hospital, Taipei 112, Taiwan.
Ching-Yin HoDepartment of Otorhinolaryngology, Taipei Veterans General Hospital, Taipei 112, Taiwan.
Wing-Yin LiDepartment of Pathology, Taipei Veterans General Hospital, Taipei 112, Taiwan.
Yann-Jang ChenDepartment of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei 112, Taiwan.
National Yang Ming Chiao Tung University · TWTaipei Veterans General Hospital · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell surface proteins such as CD44 and CD24 are used to distinguish cancer stem cells (CSCs) from the bulk-tumor population. However, the molecular functionalities of CD24 and CD44, and how these two molecules coordinate in CSCs remain poorly understood. We found that nasopharyngeal carcinoma (NPC) cells with high expression of CD44 and CD24 proteins presented with pronounced CSC properties. Accordingly, a subpopulation of NPC cells with co-expression of CD44 and CD24 were specially enriched in high-stage clinical samples. Furthermore, ectopically expressing the epithelial-mesenchymal transition (EMT) regulator Twist was able to upregulate the stemness factors, and vice versa. This indicates a reciprocal regulation of stemness and EMT. Intriguingly, we found that this reciprocal regulation was differentially orchestrated by CD44 and CD24, and only simultaneous silencing the expression of CD44 and CD24 led to a broad-spectrum suppression of CSC properties. Oppositely, overexpression of CD44 and CD24 induced the reprogramming of parental NPC cells into CSCs through STAT3 activation, which could be blunted by STAT3 inhibition, indicating that CD44 and CD24 collaboratively drive the reprogramming of NPC cells through STAT3-mediated stemness and EMT activation. Consequently, targeting of the CD44/CD24/STAT3 axis may provide a potential therapeutic paradigm for the treatment of NPC through repressing CSC activities.

Indexed as

Cellular ReprogrammingAnimalsApoptosisCarcinomaCD24 AntigenCell DifferentiationCell Line, TumorCell MembraneDose-Response Relationship, RadiationEpithelial-Mesenchymal TransitionHumansHyaluronan ReceptorsMiceMice, Inbred NODMice, SCIDNasopharyngeal CarcinomaCD24 AntigenCD24 protein, humanCD44 protein, humanHyaluronan ReceptorsSTAT3 protein, humanSTAT3 Transcription Factorcancer stem cellCD24CD44nasopharyngeal carcinomaSTAT3

Identifiers

PMID27521216
PMCPMC5295435
OpenAlexW2517527920

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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.