Evidence map›Paper›PMID 35508542›Full record

ArticleOncogene2022

RUVBL1 promotes enzalutamide resistance of prostate tumors through the PLXNA1-CRAF-MAPK pathway.

Feifei Sun, Xinpei Wang, Jing Hu, Junmei Liu, Xin Wang, Wenqiao Jia, Zeyuan Yu, Lin Gao, Baokai Dou, Ru Zhao and 8 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  5. Osteoblast-Derived ECM1 Promotes Anti-Androgen Resistance in Bone Metastatic Prostate Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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  14. [PLXNA1 is highly expressed in hepatocellular carcinoma and affects patients' survival and immune microenvironment].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023
    Article
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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

18 authors at 4 institutions in 2 countries.

Feifei SunThe Key Laboratory of Experimental Teratology, Ministry of Education and Department of Pathology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, 250012, China.ORCID http://orcid.org/0000-0001-9304-0244
Xinpei WangThe Key Laboratory of Experimental Teratology, Ministry of Education and Department of Pathology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, 250012, China.ORCID http://orcid.org/0000-0002-2304-1580
Jing HuDepartment of Pathology, Qilu Hospital, Shandong University, Jinan, 250012, China.
Junmei LiuDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Jinan, 250012, China.ORCID http://orcid.org/0000-0002-9716-3791
Xin WangThe Key Laboratory of Experimental Teratology, Ministry of Education and Department of Pathology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, 250012, China.ORCID http://orcid.org/0000-0003-1973-754X
Wenqiao JiaDepartment of Health Management Center, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250012, China.ORCID http://orcid.org/0000-0002-4510-1409
Zeyuan YuThe Key Laboratory of Experimental Teratology, Ministry of Education and Department of Pathology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, 250012, China.
Lin GaoThe Key Laboratory of Experimental Teratology, Ministry of Education and Department of Pathology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, 250012, China.ORCID http://orcid.org/0000-0002-6913-2410
Baokai DouDepartment of Pharmacy, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 250021, China.
Ru ZhaoThe Key Laboratory of Experimental Teratology, Ministry of Education and Department of Pathology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, 250012, China.ORCID http://orcid.org/0000-0001-8475-6398
Tingting FengThe Key Laboratory of Experimental Teratology, Ministry of Education and Department of Pathology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, 250012, China.ORCID http://orcid.org/0000-0002-9808-8885
Xueli WangDepartment of Pathology, Binzhou City Central Hospital, Binzhou, China.
Wenbo ZhangThe Key Laboratory of Experimental Teratology, Ministry of Education and Department of Pathology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, 250012, China.
Hui LiuDepartment of Pathology, Qilu Hospital, Shandong University, Jinan, 250012, China.
Kaihua LiuNanjing Geneseeq Technology Inc., Nanjing, Jiangsu, China.
Yang ShaoNanjing Geneseeq Technology Inc., Nanjing, Jiangsu, China.
Xuesen DongVancouver Prostate Centre, Vancouver General Hospital, Vancouver, BC, V6H 3Z6, Canada. xdong@prostatecentre.com.ORCID http://orcid.org/0000-0002-3115-3371
Bo HanThe Key Laboratory of Experimental Teratology, Ministry of Education and Department of Pathology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, 250012, China. boh@sdu.edu.cn.ORCID http://orcid.org/0000-0003-4966-1398
Shandong University · CNQilu Hospital of Shandong University · CNShandong Provincial Hospital · CNUniversity of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although enzalutamide improves the overall survival of patients with metastatic prostate cancers, enzalutamide resistance (ENZR) will be inevitably developed. Emerging evidence support that alternative oncogenic pathways may bypass the androgen receptor (AR) signaling to promote ENZR progression, however, the underpinning mechanisms remain poorly defined. Here, we report that the expression of RuvB like AAA ATPase 1 (RUVBL1) is upregulated in ENZR cells and xenograft models and prostate tumors in patients. Enzalutamide increases RUVBL1 accumulation in the cytoplasm, which in turn enhances the recruitment of CRAF proto-oncogene serine/threonine kinase protein to plexin A1 (PLXNA1) and the subsequent activation of the downstream MAPK pathway. Co-overexpression of RUVBL1 and PLXNA1 defines a subgroup of prostate cancer (PCa) patients with a poor prognosis. Furthermore, pharmacological inhibition of RUVBL1 by CB-6644 suppresses ENZR cell proliferation and xenograft growth and allows re-sensitization of ENZR cells and xenografts to enzalutamide, indicating that RUVBL1 may act to substitute the AR signaling to promote cancer cell survival and ENZR development. Together, these findings may lead to the identification of RUVBL1 as a potential therapeutic target for ENZR tumors.

Indexed as

Prostatic Neoplasms, Castration-ResistantATPases Associated with Diverse Cellular ActivitiesBenzamidesCarrier ProteinsCell Line, TumorCell ProliferationDNA HelicasesDrug Resistance, NeoplasmHumansMaleNerve Tissue ProteinsNitrilesPhenylthiohydantoinReceptors, AndrogenReceptors, Cell SurfaceATPases Associated with Diverse Cellular ActivitiesBenzamidesCarrier ProteinsDNA HelicasesenzalutamideNerve Tissue ProteinsNitrilesPhenylthiohydantoinPLXNA1 protein, humanReceptors, AndrogenReceptors, Cell SurfaceRUVBL1 protein, human

Identifiers

PMID35508542
OpenAlexW4225419660

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.