Evidence map›Paper›PMID 25713298›Full record

ArticleDisease models & mechanisms2015

Downregulation of Wnt signaling by sonic hedgehog activation promotes repopulation of human tumor cell lines.

Jingjing Ma, Jin Cheng, Yanping Gong, Ling Tian, Qian Huang

Open access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Cholesterol and Hedgehog Signaling: Mutual Regulation and Beyond.Frontiers in cell and developmental biology · 2022
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. The Sound of Silence: Signaling by Apoptotic Cells.Current topics in developmental biology · 2015
    Review
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

5 authors at 1 institution in 1 country.

Jingjing MaThe Comprehensive Cancer Center & Shanghai Key Laboratory for Pancreatic Diseases, Shanghai First People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 201620, China. Department of Pharmacy, The First Affiliated Hospital of Soochow University, Suzhou 215006, China.
Jin ChengThe Comprehensive Cancer Center & Shanghai Key Laboratory for Pancreatic Diseases, Shanghai First People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 201620, China.
Yanping GongExperimental Research Center, Shanghai First People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 201620, China.
Ling TianExperimental Research Center, Shanghai First People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 201620, China. tl09168@hotmail.com qhuang2007@gmail.com.
Qian HuangThe Comprehensive Cancer Center & Shanghai Key Laboratory for Pancreatic Diseases, Shanghai First People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 201620, China. tl09168@hotmail.com qhuang2007@gmail.com.
Shanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor repopulation after radiotherapy is a big obstacle for clinical cancer therapy. The molecular mechanisms of tumor cell repopulation after radiotherapy remain unclear. This study investigated the role of sonic hedgehog (SHH) and Wnt signaling pathways in tumor repopulation after radiotherapy in an in vitro repopulation model. In this model, irradiated dying tumor cells functioned as feeder cells, whereas luciferase-labeled living tumor cells acted as reporter cells. Proliferation of reporter cells was measured by bioluminescence imaging. Results showed that irradiated dying HT29 and Panc1 tumor cells significantly stimulated the repopulation of living cells in their respective cultures. In HT29 and Panc1 cells, radiation significantly inhibited Wnt activity. In the irradiated dying HT29 and Panc1 cells, the level of the activated nuclear β-catenin was significantly decreased. Treatment with the Wnt agonist 68166 significantly decreased, whereas treatment with Wnt antagonist significantly increased, repopulation in HT29 and Panc1 tumor cells in a dose-dependent manner. β-catenin short-hairpin RNA (shRNA) also significantly promoted tumor cell repopulation. The level of secreted frizzled related protein-1 (SFRP1), hedgehog and Gli1 were increased in irradiated cells. Our results highlight the interaction between Wnt and SHH signaling pathways in dying tumor cells and suggest that downregulation of Wnt signaling after SHH activation is negatively associated with tumor repopulation.

Indexed as

Down-RegulationWnt Signaling PathwayCell CountCell DeathCell Line, TumorCell ProliferationGene Knockdown TechniquesGenes, ReporterHedgehog ProteinsHumansLuciferasesModels, BiologicalSignal TransductionX-RaysHedgehog ProteinsLuciferasesSHH protein, humanColon cancerPancreatic cancerRadiotherapyRepopulationWnt signaling

Identifiers

PMID25713298
PMCPMC4381337
OpenAlexW2139081044

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.