Evidence map›Paper›PMID 41957134›Full record

ArticleBritish journal of cancer2026

ITGB4 up-regulated by STAT3 reduces the sensitivity of bladder cancer to cisplatin by suppressing p53.

Zhuo Xing, Haozhe Xu, Pingxia Lin, Yulong Hong, Shuai Shao, Tiejun Yang, Yuan Li, Yongbao Wei

Abstract read
In one paragraph

Article in British journal of cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. DHCR24Oncogene · 2026
    Article
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.

Zhuo Xing *Department of Urology, The Second Xiangya Hospital, Central South University, Changsha, China.
Haozhe Xu *Department of Urology, The Second Xiangya Hospital, Central South University, Changsha, China.ORCID http://orcid.org/0000-0002-7663-1533
Pingxia Lin *Department of Urology, The Second Xiangya Hospital, Central South University, Changsha, China.
Yulong HongDepartment of Urology, The Second Xiangya Hospital, Central South University, Changsha, China.
Shuai ShaoDepartment of Urology, The Second Xiangya Hospital, Central South University, Changsha, China.
Tiejun YangThe Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, China. tiejunyang@163.com.
Yuan LiDepartment of Urology, The Second Xiangya Hospital, Central South University, Changsha, China. yuanlixy@csu.edu.cn.ORCID http://orcid.org/0000-0002-5249-3172
Yongbao WeiShengli Clinical Medical College of Fujian Medical University, Fuzhou, China. weiyb@fjmu.edu.cn.ORCID http://orcid.org/0000-0003-3114-9214

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82172878National Natural Science Foundation of China (National Science Foundation of China) 82373435
6 · The paper itself

Abstract

backgroundCisplatin-based chemotherapy is the first-line treatment for patients with advanced bladder cancer (BC). However, the development of cisplatin resistance limits its antitumor effects. While, the mechanism of cisplatin resistance remains unclear.

methodsBioinformatics techniques were used to analyse genes and pathways associated with cisplatin therapy resistance. A variety of biological techniques were used to identify the role of ITGB4 in cisplatin sensitivity in BC and its potential molecular mechanism.

resultsIn this study, we demonstrated that ITGB4 plays a key role in regulating the sensitivity of p53 wild-type (WT) BC to cisplatin therapy. Our findings revealed that ITGB4 inhibits the activation of p53 by suppressing the phosphorylation at the p53-S15 site and promotes the degradation of p53 by facilitating the binding of MDM2 to p53, thereby reducing the sensitivity of BC to cisplatin.Additionally, we showed that ITGB4 influences the antitumor effects of MDM2 inhibitors when they are combined with cisplatin therapy. Furthermore, we found that the elevated expression of ITGB4 in cisplatin-resistant BC cells were mediated by STAT3 activation. The combination of STAT3 inhibitors can enhance the antitumor effect of cisplatin in BC.

conclusionsITGB4 is a key molecule influencing cisplatin sensitivity in p53 WT BC, and the combination of STAT3 inhibitors can enhance the antitumor effect of cisplatin.

Indexed as

CisplatinDrug Resistance, NeoplasmIntegrin beta4STAT3 Transcription FactorTumor Suppressor Protein p53Urinary Bladder NeoplasmsAnimalsAntineoplastic AgentsCell Line, TumorGene Expression Regulation, NeoplasticHumansPhosphorylationProto-Oncogene Proteins c-mdm2Up-RegulationAntineoplastic AgentsCisplatinIntegrin beta4ITGB4 protein, humanMDM2 protein, humanProto-Oncogene Proteins c-mdm2STAT3 protein, humanSTAT3 Transcription FactorTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID41957134
PMCPMC13226673

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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.