Evidence map›Paper›PMID 34852826›Full record

ArticleJournal of experimental & clinical cancer research : CR2021

BUB1 drives the occurrence and development of bladder cancer by mediating the STAT3 signaling pathway.

Ning Jiang, Yihao Liao, Miaomiao Wang, Youzhi Wang, Keke Wang, Jianing Guo, Peikang Wu, Boqiang Zhong, Tao Guo, Changli Wu

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 70 citations in OpenAlex.

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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

10 authors at 1 institution in 1 country.

Ning Jiang *Tianjin Institute of Urology, The Second Hospital of Tianjin Medical University, Tianjin, 300211, China. jiangning@tmu.edu.cn.ORCID http://orcid.org/0000-0002-9851-0863
Yihao Liao *Tianjin Institute of Urology, The Second Hospital of Tianjin Medical University, Tianjin, 300211, China.
Miaomiao WangTianjin Institute of Urology, The Second Hospital of Tianjin Medical University, Tianjin, 300211, China.
Youzhi WangTianjin Institute of Urology, The Second Hospital of Tianjin Medical University, Tianjin, 300211, China.
Keke WangTianjin Institute of Urology, The Second Hospital of Tianjin Medical University, Tianjin, 300211, China.
Jianing GuoDepartment of Pathology, The Second Hospital of Tianjin Medical University, Tianjin, 300211, China.
Peikang WuTianjin Institute of Urology, The Second Hospital of Tianjin Medical University, Tianjin, 300211, China.
Boqiang ZhongTianjin Institute of Urology, The Second Hospital of Tianjin Medical University, Tianjin, 300211, China.
Tao GuoTianjin Institute of Urology, The Second Hospital of Tianjin Medical University, Tianjin, 300211, China.
Changli WuTianjin Institute of Urology, The Second Hospital of Tianjin Medical University, Tianjin, 300211, China.
Second Hospital of Tianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe incidence of bladder urothelial carcinoma (UC), a common malignancy of the urinary tract, is approximately three times higher in men than in women. High expression of the mitotic kinase BUB1 is associated with the occurrence and development of several cancers, although the relationship between BUB1 and bladder tumorigenesis remains unclear.

methodsUsing a microarray approach, we found increased BUB1 expression in human BCa. The association between BUB1 and STAT3 phosphorylation was determined through molecular and cell biological methods. We evaluated the impact of pharmacologic inhibition of BUB1 kinase activity on proliferation and BCa progression in vitro and in vivo.

resultsIn this study, we found that BUB1 expression was increased in human bladder cancer (BCa). We further identified through a series of molecular and cell biological approaches that BUB1 interacted directly with STAT3 and mediated the phosphorylation of STAT3 at Ser727. In addition, the findings that pharmacologic inhibition of BUB1 kinase activity significantly suppressed BCa cell proliferation and the progression of bladder cancer in vitro and in vivo were further verified. Finally, we found that the BUB1/STAT3 complex promoted the transcription of STAT3 target genes and that depletion of BUB1 and mutation of the BUB1 kinase domain abrogated this transcriptional activity, further highlighting the critical role of kinase activity in the activation of STAT3 target genes. A pharmacological inhibitor of BUB1 (2OH-BNPP1) was able to significantly inhibit the growth of BCa cell xenografts.

conclusionThis study showed that the BUB1 kinase drives the progression and proliferation of BCa by regulating the transcriptional activation of STAT3 signaling and may be an attractive candidate for therapeutic targeting in BCa.

Indexed as

AnimalsCell ProliferationHumansMaleMicePhosphorylationProtein Serine-Threonine KinasesSignal TransductionSTAT3 Transcription FactorTransfectionUrinary Bladder NeoplasmsBub1 protein, mouseProtein Serine-Threonine KinasesStat3 protein, mouseSTAT3 Transcription FactorBladder cancerBUB1PhosphorylationProliferationSTAT3

Identifiers

PMID34852826
PMCPMC8638147
OpenAlexW3216550040

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Registered trials

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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.