Evidence map›Paper›PMID 32440342›Full record

ArticleToxicology research2020

Suppression of LINC00460 mediated the sensitization of HCT116 cells to ionizing radiation by inhibiting epithelial-mesenchymal transition.

Jiani Zhang, Lixin Ding, Gaofeng Sun, Huacheng Ning, Ruixue Huang

Open access · bronzeAbstract read
In one paragraph

Article in Toxicology research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

12 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Significance of LINC00460 in the progression and prognosis in digestive tract tumors.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2021
    Article
  11. 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

5 authors at 2 institutions in 1 country.

Jiani ZhangGerontology Department of Xiangya Hospital, Central South University, Changsha, Xiangya road 238, Hunan Province 410078, P. R. China.
Lixin DingDepartment of Radiology, National Institute for Radiological Protection, Chinese Center for Disease Control and Prevention, Taiping road 27, Beijing, 100088, P. R. China.
Gaofeng SunDepartment of Chronic and Non-communicable Diseases Control, City Center for Disease Control and Prevention, Jingyi Road 58, Urumqi, 830026, P. R. China.
Huacheng NingDepartment of Occupational and Environmental Health, Xiangya School of Public Heath, Central South University, Xiangya Road 238, Changsha, Hunan Province 410078, P. R. China.
Ruixue HuangDepartment of Occupational and Environmental Health, Xiangya School of Public Heath, Central South University, Xiangya Road 238, Changsha, Hunan Province 410078, P. R. China.
Central South University · CNNational Institute for Radiological Protection · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Radiation resistance is the most common challenge for improving radiotherapy. The mechanisms underlying the development of radioresistance remain poorly understood. This study aims to explore the role of LINC00460 in ionizing radiation-induced radioresistance as well as the mechanisms by which LINC00460 is regulated by radiation exposure. The expression of LINC00460 was measured. Cell proliferation and colony formation were measured in HCT116 cells after treatment by radiation. The development of epithelial-mesenchymal transition (EMT) was determined with or without knockdown LINC00460 expression using western blot analysis. Transcription activity was determined using a series of LINC00460-promoter luciferase reporter gene vectors. LINC00460 expression was significantly higher in HCT116 cells, relative to other cell types, with LINC00460 expression significantly affecting HCT116 cell proliferation. Suppression of LINC00460 inhibits EMT development in HCT116 cells via regulation of ZEB1 expression. Furthermore, LINC00460 expression was induced by irradiation via the activation of c-jun transcription factor-binding element located on the LINC00460 promoter. LINC00460 was shown to play a crucial role in EMT-associated progression of colorectal cancer, indicating that LINC00460 may be an indicator or new potential therapeutic target for colorectal cancer radiosensitization.

Indexed as

cancerlncRNAradiation

Identifiers

PMID32440342
PMCPMC7233317
OpenAlexW3019616517

What OpenQuestion holds

Textmetadata
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.