Evidence map›Paper›PMID 28498637›Full record

ArticleCancer science2017

β2-AR activation induces chemoresistance by modulating p53 acetylation through upregulating Sirt1 in cervical cancer cells.

Hongyu Chen, Wei Zhang, Xiang Cheng, Liang Guo, Shuai Xie, Yuanfang Ma, Ning Guo, Ming Shi

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Review
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  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. The βAdvances in pharmacological and pharmaceutical sciences · 2024
    Review
  12. Role of SIRT1 in Chemoresistant Leukemia.International journal of molecular sciences · 2023
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Observational
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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

8 authors at 2 institutions in 1 country.

Hongyu ChenInstitute of Basic Medical Sciences, Beijing, China.
Wei ZhangLaboratory of Cellular and Molecular Immunology, Medical School of Henan University, Kaifeng, China.
Xiang ChengInstitute of Basic Medical Sciences, Beijing, China.
Liang GuoInstitute of Basic Medical Sciences, Beijing, China.
Shuai XieLaboratory of Cellular and Molecular Immunology, Medical School of Henan University, Kaifeng, China.
Yuanfang MaLaboratory of Cellular and Molecular Immunology, Medical School of Henan University, Kaifeng, China.
Ning GuoInstitute of Basic Medical Sciences, Beijing, China.ORCID http://orcid.org/0000-0001-9263-6468
Ming ShiInstitute of Basic Medical Sciences, Beijing, China.
Capital Medical University · CNHenan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been suggested that β2-adrenergic receptor (β2-AR)-mediated signaling induced by catecholamines regulates the degradation of p53. However, the underlying molecular mechanisms were not known. In the present study, we demonstrated that catecholamines upregulated the expression of silent information regulator 1 (Sirt1) through activating β2-AR-mediated signaling pathway, since selective β2-AR antagonist ICI 118, 551 and non-selective β-blocker proprenolol effectively repressed isoproterenol (ISO)-induced Sirt1 expression. Catecholamines inhibited doxorubicin (DOX)-induced p53 acetylation and transcription-activation activities by inducing the expression of Sirt1. Knockdown of the Sirt1 expression by the specific siRNA remarkably blocked the inhibitory effects of ISO on DOX-induced p53 acetylation. In addition, we demonstrated that catecholamines induced resistance of cervical cancer cells to chemotherapeutics both in vitro and in vivo and that β2-AR was overexpressed in cervical cancer tissues. Our data suggest that the p53-dependent, chemotherapeutics-induced cytotoxicity in cervical cancer cells may be compromised by catecholamines-induced upregulation of the Sirt1 expression through activating the β2-AR signaling.

Indexed as

AcetylationAnimalsBlotting, WesternCatecholaminesCell Line, TumorDrug Resistance, NeoplasmFemaleGene Expression Regulation, NeoplasticHeterograftsHumansImmunohistochemistryMiceMice, Inbred BALB CMice, NudeMicroscopy, FluorescenceReal-Time Polymerase Chain ReactionCatecholaminesReceptors, Adrenergic, beta-2SIRT1 protein, humanSirtuin 1Tumor Suppressor Protein p53Cervical cancerchemoresistancep53Sirt1β2-AR

Identifiers

PMID28498637
PMCPMC5497720
OpenAlexW2613415919

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.