Evidence map›Paper›PMID 28099140›Full record

ArticleOncotarget2017

Telomerase antagonist imetelstat increases radiation sensitivity in esophageal squamous cell carcinoma.

Xuping Wu, Jing Zhang, Sijun Yang, Zhihui Kuang, Guolei Tan, Gang Yang, Qichun Wei, Zhigang Guo

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

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

8 authors at 4 institutions in 1 country.

Xuping WuThe Second Hospital of Nanjing Affiliated to Medical School of Southeast University, Nanjing 210003, China.
Jing ZhangJiangsu Key Laboratory for Molecular and Medical Biotechnology, College of Life Sciences, Nanjing Normal University, Nanjing 210023, China.
Sijun YangABSL-3 Laboratory at The Center for Animal Experiment and State Key Lab of Virology, Wuhan University, Wuhan 430071, China.
Zhihui KuangJiangsu Key Laboratory for Molecular and Medical Biotechnology, College of Life Sciences, Nanjing Normal University, Nanjing 210023, China.
Guolei TanThe Second Hospital of Nanjing Affiliated to Medical School of Southeast University, Nanjing 210003, China.
Gang YangThe Second Hospital of Nanjing Affiliated to Medical School of Southeast University, Nanjing 210003, China.
Qichun WeiDepartment of Radiation Oncology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 31009, China.
Zhigang GuoJiangsu Key Laboratory for Molecular and Medical Biotechnology, College of Life Sciences, Nanjing Normal University, Nanjing 210023, China.
Nanjing Normal University · CNSoutheast University · CNSecond Affiliated Hospital of Zhejiang University · CNWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The morbidity and mortality of esophageal cancer is one of the highest around the world and the principal therapeutic method is radiation. Thus, searching for sensitizers with lower toxicity and higher efficiency to improve the efficacy of radiation therapy is critical essential. Our research group has previously reported that imetelstat, the thio-phosphoramidate oligonucleotide inhibitor of telomerase, can decrease cell proliferation and colony formation ability as well as increase DNA breaks induced by radiation in esophageal cancer cells. Further study in this project showed that imetelstat significantly sensitized esophageal cancer cells to radiation in vitro. Later study showed that imetelstat leads to increased cell apoptosis. We also measured the expression level of several DNA repair and apoptosis signaling proteins. pS345 CHK1, γ-H2AX, p53 and caspase3 expression were up-regulated in imetelstat treated cells, identifying these factors as molecular markers. Mouse in vivo model using imetelstat at clinically achievable concentrations and fractionated irradiation scheme yielded results demonstrating radiosensitization effect. Finally, TUNEL assay, caspase 3 and Ki67 staining in tumor tissue proved that imetelstat sensitized esophageal cancer to radiation in vivo through promoting cell apoptosis and inhibiting cell proliferation. Our study supported imetelstat increase radiation sensitivity of esophageal squamous cell carcinoma through inducing cell apoptosis and the specific inhibitor of telomerase might serve as a potential novel therapeutic tool for esophageal squamous cell carcinoma therapy.

Indexed as

AnimalsApoptosisCarcinoma, Squamous CellEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaHumansIndolesMaleMiceMice, NudeNiacinamideOligonucleotidesRandom AllocationTelomeraseXenograft Model Antitumor AssaysimetelstatIndolesNiacinamideOligonucleotidesTelomeraseapoptosisesophageal squamous cell carcinomaradiosensitizationtelomerase

Identifiers

PMID28099140
PMCPMC5355123
OpenAlexW2577431949

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.