Evidence map›Paper›PMID 30166523›Full record

ArticleCell death & disease2018

CD59 is a potential biomarker of esophageal squamous cell carcinoma radioresistance by affecting DNA repair.

Yuzhen Zhou, Li Chu, Qi Wang, Weixing Dai, Xiaozhou Zhang, Jianfeng Chen, Ling Li, Peipei Ding, Long Zhang, Hongyu Gu and 8 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

29 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Radiotherapy resistance: identifying universal biomarkers for various human cancers.Journal of cancer research and clinical oncology · 2022
    Review
  15. Article
  16. Association of Blood Group Antigen CD59 with Disease.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2022
    Review
  17. Article
  18. Article
  19. Article
  20. Targeting the Complement Pathway in Malignant Glioma Microenvironments.Frontiers in cell and developmental biology · 2021
    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

18 authors at 2 institutions in 1 country.

Yuzhen ZhouFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, 200032, Shanghai, China.
Li ChuDepartment of Radiation Oncology, Fudan University Shanghai Cancer Center, Shanghai Medical College, Fudan University, 200032, Shanghai, China.
Qi WangFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, 200032, Shanghai, China.
Weixing DaiDepartment of Colorectal Surgery, Shanghai Medical College, Fudan University, 200032, Shanghai, China.
Xiaozhou ZhangFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, 200032, Shanghai, China.
Jianfeng ChenFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, 200032, Shanghai, China.
Ling LiFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, 200032, Shanghai, China.
Peipei DingFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, 200032, Shanghai, China.
Long ZhangFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, 200032, Shanghai, China.
Hongyu GuFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, 200032, Shanghai, China.
Luying LiFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, 200032, Shanghai, China.
Xinyue LvFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, 200032, Shanghai, China.
Wei ZhangFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, 200032, Shanghai, China.
Danlei ZhouFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, 200032, Shanghai, China.
Pingzhao ZhangFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, 200032, Shanghai, China.
Guoxiang CaiDepartment of Colorectal Surgery, Shanghai Medical College, Fudan University, 200032, Shanghai, China.
Kuaile ZhaoDepartment of Radiation Oncology, Fudan University Shanghai Cancer Center, Shanghai Medical College, Fudan University, 200032, Shanghai, China. dyzhao@fudan.edu.cn.
Weiguo HuFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, 200032, Shanghai, China. weiguohu@fudan.edu.cn.ORCID 0000-0002-7397-6800
Fudan University Shanghai Cancer Center · CNShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Radiation therapy is an important treatment modality for esophageal cancer. However, acquisition of radioresistance ultimately results in esophageal cancer relapse. CD59, a membrane-bound complement regulatory protein, can transduce signals via a Src kinase in the lipid raft, thus playing a complement-independent role. However, the effect of CD59 on the esophageal cancer response to ionizing radiation remains unclear. In this study, we found that the expression level of CD59 was positively correlated with the radioresistance of esophageal cancer cell lines and clinical specimens. High CD59 expression indicated poor overall survival (OS) and disease-free survival (DFS) in esophageal squamous cell carcinoma (ESCC) patients who received radiotherapy. Genetic alteration of CD59 expression modulated the radiosensitivity of esophageal cancer cells to ionizing radiation. CD59 deficiency exacerbated DNA damage, hindered cell proliferation, and induced G2/M cell cycle arrest and cellular senescence, leading to an impaired DNA damage repair ability. In addition, CD59 deficiency almost completely reduced the phosphorylation of Src at Y416 despite ionizing radiation. A Src inhibitor saracatinib sensitized esophageal cancer cells to irradiation. Therefore, CD59 may be a potential biomarker for predicting the radioresistance of ESCC to radiotherapy.

Indexed as

AnimalsBenzodioxolesBiomarkers, TumorCD59 AntigensCell Line, TumorCell ProliferationCellular SenescenceDisease-Free SurvivalDNA DamageDNA RepairEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaG2 Phase Cell Cycle CheckpointsHumansMiceMice, Inbred BALB CBenzodioxolesBiomarkers, TumorCD59 AntigensCD59 protein, humanQuinazolinessaracatinib

Identifiers

PMID30166523
PMCPMC6117325
OpenAlexW2888843273

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.