Evidence map›Paper›PMID 24349176›Full record

ArticlePloS one2013

Celecoxib-induced cytotoxic effect is potentiated by inhibition of autophagy in human urothelial carcinoma cells.

Kuo-How Huang, Kuan-Lin Kuo, I-Lin Ho, Hong-Chiang Chang, Yuan-Ting Chuang, Wei-Chou Lin, Ping-Yi Lee, Shih-Chen Chang, Chih-Kang Chiang, Yeong-Shiau Pu and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

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  7. The Akt pathway in oncology therapy and beyond (Review).International journal of oncology · 2018
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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

13 authors at 2 institutions in 1 country.

Kuo-How HuangGraduate institute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan ; Department of Urology, National Taiwan University Hospital, Taipei, Taiwan.
Kuan-Lin KuoDepartment of Urology, National Taiwan University Hospital, Taipei, Taiwan.
I-Lin HoDepartment of Urology, National Taiwan University Hospital, Taipei, Taiwan.
Hong-Chiang ChangDepartment of Urology, National Taiwan University Hospital, Taipei, Taiwan.
Yuan-Ting ChuangDepartment of Urology, National Taiwan University Hospital, Taipei, Taiwan.
Wei-Chou LinDepartment of Pathology, National Taiwan University Hospital, Taipei, Taiwan.
Ping-Yi LeeDepartment of Urology, National Taiwan University Hospital, Taipei, Taiwan.
Shih-Chen ChangDepartment of Urology, National Taiwan University Hospital, Taipei, Taiwan ; Department of Chemical Engineering, College of Engineering, National Taiwan University, Taipei, Taiwan.
Chih-Kang ChiangDepartment of Integrated Diagnostics and Therapeutics, National Taiwan University Hospital, Taipei, Taiwan.
Yeong-Shiau PuDepartment of Urology, National Taiwan University Hospital, Taipei, Taiwan.
Chien-Tso ChouDepartment of Urology, National Taiwan University Hospital, Taipei, Taiwan.
Chen-Hsun HsuDepartment of Urology, National Taiwan University Hospital, Taipei, Taiwan.
Shing-Hwa LiuGraduate institute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan.
National Taiwan University Hospital · TWNational Taiwan University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Celecoxib, a cyclooxygenase-2 (COX-2) inhibitor, can elicit anti-tumor effects in various malignancies. Here, we sought to clarify the role of autophagy in celecoxib-induced cytotoxicity in human urothelial carcinoma (UC) cells. The results shows celecoxib induced cellular stress response such as endoplasmic reticulum (ER) stress, phosopho-SAPK/JNK, and phosopho-c-Jun as well as autophagosome formation in UC cells. Inhibition of autophagy by 3-methyladenine (3-MA), bafilomycin A1 or ATG7 knockdown potentiated celecoxib-induced apoptosis. Up-regulation of autophagy by rapamycin or GFP-LC3B-transfection alleviated celecoxib-induced cytotoxicity in UC cells. Taken together, the inhibition of autophagy enhances therapeutic efficacy of celecoxib in UC cells, suggesting a novel therapeutic strategy against UC.

Indexed as

Gene Expression Regulation, NeoplasticAdenineAntineoplastic AgentsAutophagyAutophagy-Related Protein 7Carcinoma, Transitional CellCelecoxibCell Line, TumorCyclooxygenase 2 InhibitorsEndoplasmic Reticulum StressHumansJNK Mitogen-Activated Protein KinasesMacrolidesMAP Kinase Kinase 4PhosphoproteinsPyrazoles3-methyladenineAdenineAntineoplastic AgentsATG7 protein, humanAutophagy-Related Protein 7bafilomycin A1CelecoxibCyclooxygenase 2 InhibitorsJNK Mitogen-Activated Protein KinasesMacrolidesMAP Kinase Kinase 4PhosphoproteinsPyrazolesRNA, Small InterferingSirolimusSulfonamidesUbiquitin-Activating Enzymes

Identifiers

PMID24349176
PMCPMC3857231
OpenAlexW2040123739

What OpenQuestion 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 OpenQuestion graph.