Evidence map›Paper›PMID 33546743›Full record

ArticleCell & bioscience2021

Transcriptomic and metabolomic profiling reveal the p53-dependent benzeneacetic acid attenuation of silica-induced epithelial-mesenchymal transition in human bronchial epithelial cells.

Zhao Ju, Jianlin Shao, Meiling Zhou, Jing Jin, Huiji Pan, Ping Ding, Ruixue Huang

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 30% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Engineering microbiology · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Inhaled toxicants and pulmonary lipid metabolism: biological consequences and therapeutic interventions.Toxicological sciences : an official journal of the Society of Toxicology · 2023
    Article
  11. 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

7 authors at 2 institutions in 1 country.

Zhao JuDepartment of Occupational and Environmental Health, Xiangya School of Public Health, Central South University, Changsha, 410078, Hunan, China.
Jianlin ShaoZhejiang Provincial Center for Cardiovascular Disease Prevention and Control, Zhejiang Hospital, Hangzhou, Zhejiang, China.
Meiling ZhouDepartment of Occupational and Environmental Health, Xiangya School of Public Health, Central South University, Changsha, 410078, Hunan, China.
Jing JinDepartment of Occupational and Environmental Health, Xiangya School of Public Health, Central South University, Changsha, 410078, Hunan, China.
Huiji PanDepartment of Occupational and Environmental Health, Xiangya School of Public Health, Central South University, Changsha, 410078, Hunan, China.
Ping DingDepartment of Occupational and Environmental Health, Xiangya School of Public Health, Central South University, Changsha, 410078, Hunan, China.
Ruixue HuangDepartment of Occupational and Environmental Health, Xiangya School of Public Health, Central South University, Changsha, 410078, Hunan, China. huangruixue@csu.edu.cn.
Central South University · CNZhejiang Center for Disease Control and Prevention · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSilica exposure underlies the development of silicosis, one of the most serious occupational hazards worldwide. We aimed to explore the interaction of the silica-induced epithelial-mesenchymal transition (EMT)-related transcripts with the cellular metabolism regulated by p53.

methodsWe knocked out p53 using CRISPR/Cas9 in the human bronchial epithelial (HBE) cell line. The transcriptomic and metabolomic analyses and integrative omics were conducted using microarrays, GC-MS, and MetaboAnalyst, respectively.

resultsFifty-two mRNAs showed significantly altered expression in the HBE p53-KO cells post-silica exposure. A total of 42 metabolites were putatively involved in p53-dependent silica-mediated HBE cell dysfunction. Through integrated data analysis, we obtained five significant p53-dependent metabolic pathways including phenylalanine, glyoxylate, dicarboxylate, and linoleic acid metabolism, and the citrate cycle. Through metabolite screening, we further identified that benzeneacetic acid, a key regulation metabolite in the phenylalanine metabolic pathway, attenuated the silica-induced EMT in HBE cells in a p53-dependent manner. Interestingly, despite the extensive p53-related published literature, the clinical translation of these studies remains unsubstantial.

conclusionsOur study offers new insights into the molecular mechanisms by which epithelial cells respond to silica exposure and provide fresh perspective and direction for future clinical biomarker research and potential clinically sustainable and translatable role of p53.

Indexed as

EMTp53Silica

Identifiers

PMID33546743
PMCPMC7866764
OpenAlexW3126424407

What Socratic 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 Socratic graph.