Evidence map›Paper›PMID 32318262›Full record

ArticleCell & bioscience2020

Integrated analysis of transcriptomic and metabolomic profiling reveal the p53 associated pathways underlying the response to ionizing radiation in HBE cells.

Ruixue Huang, Xiaodan Liu, He Li, Yao Zhou, Ping-Kun Zhou

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2020. 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
2.4field-weighted citation impact, top 10% 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, 37 citations in OpenAlex.

  1. Article
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  8. Role of p53 in Regulating Radiation Responses.Life (Basel, Switzerland) · 2022
    Review
  9. Review
  10. Article
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  12. Identification of Small Airway Epithelium-Related Hub Genes in Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2022
    Article
  13. Review
  14. 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.

Ruixue Huang1Department of Occupational and Environmental Health, Xiangya School of Public Health, Central South University, Changsha, Hunan 410078 China.
Xiaodan LiuDepartment of Radiation Biology, Beijing Key Laboratory for Radiobiology, Beijing Institute of Radiation Medicine, AMMS, Beijing, 100850 China.
He Li1Department of Occupational and Environmental Health, Xiangya School of Public Health, Central South University, Changsha, Hunan 410078 China.
Yao Zhou1Department of Occupational and Environmental Health, Xiangya School of Public Health, Central South University, Changsha, Hunan 410078 China.
Ping-Kun ZhouDepartment of Radiation Biology, Beijing Key Laboratory for Radiobiology, Beijing Institute of Radiation Medicine, AMMS, Beijing, 100850 China.
Central South University · CNBeijing Radiation Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRadiation damage to normal tissues is a serious concern. P53 is a well-known transcription factor which is closely associated with radiation-induced cell damage. Increasing evidence has indicated that regulation of metabolism by p53 represents a reviving mechanism vital to protect cell survival. We aimed to explore the interactions of radiation-induced transcripts with the cellular metabolism regulated by p53.

methodsHuman bronchial epithelial (HBE) cell line was used to knockout p53 using CRISPR/cas9. Transcriptomic analysis was conducted by microarray and metabolomic analysis was conducted by GC-MS. Integrative omics was performed using MetaboAnalyst.

results326 mRNAs showed significantly altered expression in HBE p53-/- cells post-radiation, of which 269 were upregulated and 57 were downregulated. A total of 147 metabolites were altered, including 45 that increased and 102 that decreased. By integrated analysis of both omic data, we found that in response to radiation insult, nitrogen metabolism, glutathione metabolism, arachidonic acid metabolism, and glycolysis or gluconeogenesis may be dysregulated due to p53.

conclusionsOur study provided a pilot comprehensive view of the metabolism regulated by p53 in response to radiation exposure. Detailed evaluation of these important p53-regulated metabolic pathways, including their roles in the response to radiation of cells, is essential to elucidate the molecular mechanisms of radiation-induced damage.

Identifiers

PMID32318262
PMCPMC7160934
OpenAlexW3017000664

What Socratic holds

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LicenceCC BY
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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 Socratic graph.