Evidence map›Paper›PMID 25888911›Full record

ArticleJournal of translational medicine2015

FH535 increases the radiosensitivity and reverses epithelial-to-mesenchymal transition of radioresistant esophageal cancer cell line KYSE-150R.

Huafang Su, Xiance Jin, Xuebang Zhang, Lihao Zhao, Baochai Lin, Lili Li, Zhenghua Fei, Lanxiao Shen, Ya Fang, Huanle Pan and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

40 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. 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

11 authors at 1 institution in 1 country.

Huafang SuRadiotherapy and Chemotherapy Deparment, the 1st Affiliated Hospital of Wenzhou Medical University, No.2 Fuxue Lane, 325000, Wenzhou, China. 12602639@qq.com.
Xiance JinRadiotherapy and Chemotherapy Deparment, the 1st Affiliated Hospital of Wenzhou Medical University, No.2 Fuxue Lane, 325000, Wenzhou, China. jinxc1979@hotmail.com.
Xuebang ZhangRadiotherapy and Chemotherapy Deparment, the 1st Affiliated Hospital of Wenzhou Medical University, No.2 Fuxue Lane, 325000, Wenzhou, China. baxuza@126.com.
Lihao ZhaoRadiotherapy and Chemotherapy Deparment, the 1st Affiliated Hospital of Wenzhou Medical University, No.2 Fuxue Lane, 325000, Wenzhou, China. zlh0577@gmail.com.
Baochai LinRadiotherapy and Chemotherapy Deparment, the 1st Affiliated Hospital of Wenzhou Medical University, No.2 Fuxue Lane, 325000, Wenzhou, China. chaichaiwz@163.com.
Lili LiRadiotherapy and Chemotherapy Deparment, the 1st Affiliated Hospital of Wenzhou Medical University, No.2 Fuxue Lane, 325000, Wenzhou, China. lovelydowndown@126.com.
Zhenghua FeiRadiotherapy and Chemotherapy Deparment, the 1st Affiliated Hospital of Wenzhou Medical University, No.2 Fuxue Lane, 325000, Wenzhou, China. hui-y@163.com.
Lanxiao ShenRadiotherapy and Chemotherapy Deparment, the 1st Affiliated Hospital of Wenzhou Medical University, No.2 Fuxue Lane, 325000, Wenzhou, China. 337612340@qq.com.
Ya FangRadiotherapy and Chemotherapy Deparment, the 1st Affiliated Hospital of Wenzhou Medical University, No.2 Fuxue Lane, 325000, Wenzhou, China. fangyafy@126.com.
Huanle PanRadiotherapy and Chemotherapy Deparment, the 1st Affiliated Hospital of Wenzhou Medical University, No.2 Fuxue Lane, 325000, Wenzhou, China. phlphh@163.com.
Congying XieRadiotherapy and Chemotherapy Deparment, the 1st Affiliated Hospital of Wenzhou Medical University, No.2 Fuxue Lane, 325000, Wenzhou, China. wzxiecongying@163.com.
Wenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcquired radioresistance has significantly compromised the efficacy of radiotherapy for esophageal cancer. The purpose of this study is to investigate the roles of epithelial-mesenchymal transition (EMT) and the Wnt/β-catenin signaling pathway in the acquirement of radioresistance during the radiation treatment of esophageal cancer.

methodsWe previously established a radioresistant cell line (KYSE-150R) from the KYSE-150 cell line (a human cell line model for esophageal squamous cell carcinoma) with a gradient cumulative irradiation dose. In this study, the expression of EMT phenotypes and the Wnt/β-catenin signaling pathway proteins were examined by real-time PCR, western blot and immunofluorescence in the KYSE-150R cells. The KYSE-150R cells were then treated with a β-Catenin/Tcf inhibitor FH535. The expressions of nuclear and cytoplasmic β-catenin and EMT markers in KYSE-150R cells were assessed at both mRNA and protein level after FH535 treatment. The radiosensitization effect of FH535 on KYSE-150R was evaluated by CCK8 analysis and a colony forming assay. DNA repair capacities was detected by the neutral comet assays.

resultsKYSE-150R cell line displayed obvious radiation resistance and had a stable genetic ability. EMT phenotype was presented in the KYSE-150R cells with decreased E-cadherin and increased snail and twist expressions. The up-regulated expressions of Wnt/β-catenin signaling pathway proteins (Wnt1, FZD1-4, GSK3β, CTNNB1 and Cyclin D1), the increased phosphorylation of GSK3β, and the decreased phosphorylation of β-catenin were observed in KYSE-150R cells compared with KYSE-150 cells, implicating the activation of the Wnt pathway in KYSE-150R cells. The expression of nuclear β-catenin and nuclear translocation of β-catenin from the cytoplasm was decreased after FH535 treatment. FH535 also reversed EMT phenotypes by increasing E-cadherin expression. The cell proliferation rates of KYSE-150R were dose-dependent and the radiation survival fraction was significantly decreased upon FH535 treatment. Neutral comet assays indicated that FH535 impairs DNA double stranded break repair in KYSE-150R cells.

conclusionsAcquisition of radioresistance and EMT in esophageal cancer cells is associated with the activation of the Wnt/β-catenin pathway. EMT phenotypes can be reduced and the radiosensitivity of esophageal cancer cells can be enhanced by inhibiting the Wnt/β-catenin pathway with FH535 treatment.

Indexed as

beta CateninCarcinoma, Squamous CellCell Line, TumorCell NucleusCell SurvivalEpithelial-Mesenchymal TransitionEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaHumansPhenotypeProtein TransportRadiation-Sensitizing AgentsRadiation ToleranceSulfonamidesWnt Signaling Pathwaybeta CateninFH535Radiation-Sensitizing AgentsSulfonamides

Identifiers

PMID25888911
PMCPMC4384308
OpenAlexW2164917981

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.