Evidence map›Paper›PMID 33261027›Full record

ArticleInternational journal of molecular sciences2020

E2F1 Promotes Progression of Bladder Cancer by Modulating RAD54L Involved in Homologous Recombination Repair.

Jeong-Yeon Mun, Seung-Woo Baek, Won Young Park, Won-Tae Kim, Seon-Kyu Kim, Yun-Gil Roh, Mi-So Jeong, Gi-Eun Yang, Jong-Ho Lee, Jin Woong Chung and 3 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 36 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

13 authors at 5 institutions in 1 country.

Jeong-Yeon MunDepartment of Biological Sciences, Dong-A University, Busan 49315, Korea.
Seung-Woo BaekDepartment of Bioinformatics, KRIBB School of Bioscience, Korea University of Science and Technology, Daejeon 34113, Korea.
Won Young ParkDepartment of Pathology, Pusan National University Hospital, Busan 49241, Korea.
Won-Tae KimDepartment of Biological Sciences, Dong-A University, Busan 49315, Korea.
Seon-Kyu KimDepartment of Bioinformatics, KRIBB School of Bioscience, Korea University of Science and Technology, Daejeon 34113, Korea.ORCID 0000-0002-4176-5187
Yun-Gil RohDepartment of Biological Sciences, Dong-A University, Busan 49315, Korea.
Mi-So JeongDepartment of Biological Sciences, Dong-A University, Busan 49315, Korea.
Gi-Eun YangDepartment of Biological Sciences, Dong-A University, Busan 49315, Korea.
Jong-Ho LeeDepartment of Biological Sciences, Dong-A University, Busan 49315, Korea.
Jin Woong ChungDepartment of Biological Sciences, Dong-A University, Busan 49315, Korea.
Yung Hyun ChoiDepartment of Biochemistry, College of Korean Medicine, Dong-eui University, Busan 47227, Korea.ORCID 0000-0002-1454-3124
In-Sun ChuDepartment of Bioinformatics, KRIBB School of Bioscience, Korea University of Science and Technology, Daejeon 34113, Korea.
Sun-Hee LeemDepartment of Biological Sciences, Dong-A University, Busan 49315, Korea.
Dong-A University · KRKorea Research Institute of Bioscience and Biotechnology · KRDong-Eui University · KRDongnam Institute of Radiological & Medical Sciences · KRPusan National University Hospital · KR

Funding

National Research Foundation of Korea 2020R1A2C1007356
6 · The paper itself

Abstract

DNA repair defects are important factors in cancer development. High DNA repair activity can affect cancer progression and chemoresistance. DNA double-strand breaks in cancer cells caused by anticancer agents can be restored by non-homologous end joining (NHEJ) and homologous recombination repair (HRR). Our previous study has identified E2F1 as a key gene in bladder cancer progression. In this study, DNA repair genes related to E2F1 were analyzed, and RAD54L involved in HRR was identified. In gene expression analysis of bladder cancer patients, the survival of patients with high RAD54L expression was shorter with cancer progression than in patients with low RAD54L expression. This study also revealed that E2F1 directly binds to the promoter region of RAD54L and regulates the transcription of RAD54L related to the HRR pathway. This study also confirmed that DNA breaks are repaired by RAD54L induced by E2F1 in bladder cancer cells treated with MMC. In summary, RAD54L was identified as a new target directly regulated by E2F1. Our results suggest that, E2F1 and RAD54L could be used as diagnostic markers for bladder cancer progression and represent potential therapeutic targets.

Indexed as

Disease ProgressionRecombinational DNA RepairBase SequenceCell Line, TumorDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA HelicasesE2F1 Transcription FactorGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMitomycinPrognosisTranscriptional ActivationUrinary Bladder NeoplasmsDNA-Binding ProteinsDNA HelicasesE2F1 protein, humanE2F1 Transcription FactorMitomycinRAD54L protein, humanbladder cancerE2F1homologous recombination repairprognostic biomarkersRAD54L

Identifiers

PMID33261027
PMCPMC7730422
OpenAlexW3108339828

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.