Evidence map›Paper›PMID 22859938›Full record

ArticlePloS one2012

Endoplasmic reticulum stress stimulates p53 expression through NF-κB activation.

Wan-Chi Lin, Yu-Chi Chuang, Yung-Sheng Chang, Ming-Derg Lai, Yen-Ni Teng, Ih-Jen Su, Clay C C Wang, Kuan-Han Lee, Jui-Hsiang Hung

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

53 citing papers in PubMed, 105 citations in OpenAlex.

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  14. Expression of Human Mutant Preproinsulins Induced Unfolded Protein Response,International journal of molecular sciences · 2021
    Article
  15. Article
  16. The regulatory roles of p53 in cardiovascular health and disease.Cellular and molecular life sciences : CMLS · 2021
    Review
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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

9 authors at 6 institutions in 2 countries.

Wan-Chi LinEppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, Nebraska, United States of America.
Yu-Chi Chuang
Yung-Sheng Chang
Ming-Derg Lai
Yen-Ni Teng
Ih-Jen Su
Clay C C Wang
Kuan-Han Lee
Jui-Hsiang Hung
National Cheng Kung University · TWChia Nan University of Pharmacy and Science · TWNational Health Research Institutes · TWNational University of Tainan · TWUniversity of Nebraska Medical Center · USUniversity of Southern California · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInduction of apoptosis by endoplasmic reticulum (ER) stress is implicated as the major factor in the development of multiple diseases. ER stress also appears to be a potentially useful major response to many chemotherapeutic drugs and environmental chemical compounds. A previous study has indicated that one major apoptotic regulator, p53, is significantly increased in response to ER stress, and participates in ER stress-induced apoptosis. However, the regulators of p53 expression during ER stress are still not fully understood. PRINCIPAL

findingsIn this report, we demonstrate that induction of p53 expression is mediated through NF-κB signaling pathways during ER stress in MCF-7 cells. Tunicamycin or brefeldin A, two ER stress inducers, increased p53 expression in MCF-7 and Hela cells. We found p53 nuclear localization, activity, and phosphorylation at serine 15 on p53 increased during ER stress. Nuclear translocation of NF-κB and activity of NF-κB were also observed during ER stress. ER stress-induced p53 expression was significantly inhibited by coincubation with the NF-κB inhibitor, Bay 11-7082 and downregulation of NF-κB p65 expression. The role of p53 in mediating Brefeldin A-induced apoptosis was also investigated. Induction of p53 expression by Brefeldin A was correlated to Brefeldin A-induced apoptosis. Furthermore, downregulation of p53 expression by p53 siRNA significantly reduced Brefeldin A-induced apoptosis in MCF-7 cells. SIGNIFICANCE: Taken together, NF-κB activation and induction of p53 expression is essential for ER stress-induced cell death which is important for therapeutic effects of clinical cancer drugs. Our results may provide insight into the mechanism of cancer chemotherapy efficacy that is associated with induction of ER stress.

Indexed as

Endoplasmic Reticulum StressTranscriptional ActivationApoptosisBrefeldin ACycloheximideDactinomycinGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHCT116 CellsHeLa CellsHumansMCF-7 CellsNF-kappa BPhosphorylationProtein Processing, Post-TranslationalProtein Synthesis InhibitorsBrefeldin ACycloheximideDactinomycinGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaNF-kappa BProtein Synthesis InhibitorsTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID22859938
PMCPMC3408479
OpenAlexW2020353664

What OpenQuestion 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 OpenQuestion graph.