Evidence map›Paper›PMID 34650035›Full record

ArticleCell death & disease2021

The FOXM1/RNF26/p57 axis regulates the cell cycle to promote the aggressiveness of bladder cancer.

Lu Yi, Haohui Wang, Wei Li, Kun Ye, Wei Xiong, Haixin Yu, Xin Jin

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.8field-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

23 citing papers in PubMed, 39 citations in OpenAlex.

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  13. FOXM1 promotes TGF-β2-induced injury of human lens epithelial cells by up regulating VEGFA expression.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2023
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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

7 authors at 2 institutions in 1 country.

Lu Yi *Department of Urology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China.
Haohui Wang *Department of Urology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China.
Wei LiDepartment of Urology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China.
Kun YeUro-Oncology Institute of Central South University, Changsha, Hunan, 410011, China.
Wei XiongDepartment of Urology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China.
Haixin YuCancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. haixin.y@outlook.com.ORCID 0000-0002-0245-2102
Xin JinDepartment of Urology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China. jinxinxy2@csu.edu.cn.ORCID 0000-0001-6461-6005
Central South University · CNUnion Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bladder cancer is one of the most lethal cancers in the world. Despite the continuous development of medical technologies and therapeutic strategies, the overall survival rate of bladder cancer has not changed significantly. Targeted therapy is a new promising method for bladder cancer treatment. Thus, an in-depth study of the molecular mechanism of the occurrence and development of bladder cancer is urgently needed to identify novel therapeutic candidates for bladder cancer. Here, bioinformatics analysis demonstrated that RNF26 was one of the risk factors for bladder cancer. Then, we showed that RNF26 is abnormally upregulated in bladder cancer cells and tissues and that higher RNF26 expression is an unfavorable prognostic factor for bladder cancer. Moreover, we found that RNF26 promotes bladder cancer progression. In addition, we showed that RNF26 expression is promoted by FOXM1 at the transcriptional level through MuvB complex. The upregulated RNF26 in turn degrades p57 (CDKN1C) to regulate the cell cycle process. Collectively, we uncovered a novel FOXM1/RNF26/p57 axis that modulates the cell cycle process and enhances the progression of bladder cancer. Thus, the FOXM1/RNF26/p57 signaling axis could be a candidate target for the treatment of bladder cancer.

Indexed as

Cell CycleSignal TransductionCell Line, TumorCell ProliferationCyclin-Dependent Kinase Inhibitor p57Disease ProgressionForkhead Box Protein M1Gene Expression Regulation, NeoplasticHumansModels, BiologicalNeoplasm InvasivenessNeoplasm ProteinsPrognosisProtein BindingUp-RegulationUrinary Bladder NeoplasmsCDKN1C protein, humanCyclin-Dependent Kinase Inhibitor p57Forkhead Box Protein M1Neoplasm ProteinsRNF26 protein, human

Identifiers

PMID34650035
PMCPMC8516991
OpenAlexW3206264329

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.