Evidence map›Paper›PMID 25980501›Full record

ArticleOncotarget2015

Wnt-C59 arrests stemness and suppresses growth of nasopharyngeal carcinoma in mice by inhibiting the Wnt pathway in the tumor microenvironment.

Yue Cheng, Yee Peng Phoon, Xiwan Jin, Shing Yee Steffi Chong, Joseph Chok Yan Ip, Bonnie Wing Yan Wong, Maria Li Lung

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 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

39 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
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  10. The role of Evi/Wntless in exporting Wnt proteins.Development (Cambridge, England) · 2023
    Review
  11. Wnt Signaling Pathways: From Inflammation to Non-Melanoma Skin Cancers.International journal of molecular sciences · 2023
    Review
  12. Wnt/β-catenin signaling in cancers and targeted therapies.Signal transduction and targeted therapy · 2021
    Review
  13. Wnt-C59 inhibits proinflammatory cytokine expression by reducing the interaction between β-catenin and NF-κB in LPS-stimulated epithelial and macrophage cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021
    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

7 authors at 1 institution in 1 country.

Yue ChengDepartment of Clinical Oncology, Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Laboratory Block, Pokfulam, Hong Kong SAR, China.
Yee Peng PhoonDepartment of Clinical Oncology, Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Laboratory Block, Pokfulam, Hong Kong SAR, China.
Xiwan JinDepartment of Clinical Oncology, Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Laboratory Block, Pokfulam, Hong Kong SAR, China.
Shing Yee Steffi ChongDepartment of Clinical Oncology, Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Laboratory Block, Pokfulam, Hong Kong SAR, China.
Joseph Chok Yan IpDepartment of Clinical Oncology, Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Laboratory Block, Pokfulam, Hong Kong SAR, China.
Bonnie Wing Yan WongDepartment of Clinical Oncology, Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Laboratory Block, Pokfulam, Hong Kong SAR, China.
Maria Li LungDepartment of Clinical Oncology, Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Laboratory Block, Pokfulam, Hong Kong SAR, China.
University of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Wnt/β-catenin signaling is responsible for the generation of cancer stem cells (CSCs) in many human tumors, including nasopharyngeal carcinoma (NPC). Recent studies demonstrate that Wnt or PORCN inhibitor, Wnt-C59, inhibits tumor growth in MMTV-WNT1 transgenic mice. The effect of Wnt-C59 in human tumors is not clear. In this study, the NPC cell lines investigated manifest heterogeneous responses to Wnt-C59 treatment. Wnt-C59 decreased tumor growth of SUNE1 cells in mice immediately following the administration of Wnt-C59. Mice injected with HNE1 cells did not develop visible tumors after the treatment of Wnt-C59, while control mice developed 100% tumors. Wnt-C59 inhibited stemness properties of NPC cells in a dosage-dependent manner by arresting sphere formation in both HNE1 and SUNE1 cells. Thus, Wnt-C59 has the potential to eradicate CSCs in human tumors. Active β-catenin and Axin2 proteins were strongly expressed in stromal cells surrounding growing tumors, confirming the importance of Wnt signaling activities in the microenvironment being driving forces for cell growth. These novel findings confirm the ability of Wnt-C59 to suppress Wnt-driven undifferentiated cell growth in NPC. Both anti-Wnt signaling and anti-CSC approaches are feasible strategies in cancer therapy.

Indexed as

AnimalsCarcinomaCell Line, TumorCell ProliferationGenes, Tumor SuppressorHumansImmunohistochemistryMiceNasopharyngeal CarcinomaNasopharyngeal NeoplasmsNeoplastic Stem CellsTumor MicroenvironmentWnt Signaling Pathwaycancer stem cellsnasopharyngeal carcinomatumor suppressionWnt-C59Wnt pathway

Identifiers

PMID25980501
PMCPMC4546477
OpenAlexW1771639668

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.