Evidence map›Paper›PMID 33087165›Full record

ArticleJournal of experimental & clinical cancer research : CR2020

Activation of the KDM5A/miRNA-495/YTHDF2/m6A-MOB3B axis facilitates prostate cancer progression.

Chen Du, Caihong Lv, Yue Feng, Siwen Yu

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
5.1field-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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

  1. Pooled it
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  8. mActa pharmaceutica Sinica. B · 2025
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  10. WTAP-mediated mScience China. Life sciences · 2025
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7 more citing papers are in PubMed but not listed here.

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

4 authors at 3 institutions in 1 country.

Chen DuDepartment of Urology Surgery, Harbin Medical University Cancer Hospital, No. 150, Haping Road, Nangang District, Harbin, 150000, Heilongjiang Province, People's Republic of China. Duchen0707@126.com.
Caihong LvDepartment of Laboratory, the Fourth Affiliated Hospital of Harbin Medical University, Harbin, 150001, People's Republic of China.
Yue FengDepartment of Urology Surgery, Harbin Medical University Cancer Hospital, No. 150, Haping Road, Nangang District, Harbin, 150000, Heilongjiang Province, People's Republic of China.
Siwen YuDepartment of Urology Surgery, Harbin Medical University Cancer Hospital, No. 150, Haping Road, Nangang District, Harbin, 150000, Heilongjiang Province, People's Republic of China.
Third Affiliated Hospital of Harbin Medical University · CNFourth Affiliated Hospital of Harbin Medical University · CNHarbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAccumulating evidence supports that lysine-specific demethylase 5 (KDM5) family members act as oncogenic drivers. This study was performed to elucidate the potential effects of KDM5A on prostate cancer (PCa) progression via the miR-495/YTHDF2/m6A-MOB3B axis.

methodsThe expression of KDM5A, miR-495, YTHDF2 and MOB3B was validated in human PCa tissues and cell lines. Ectopic expression and knockdown experiments were developed in PCa cells to evaluate their effects on PCa cell proliferation, migration, invasion and apoptosis. Mechanistic insights into the interaction among KDM5A, miR-495, YTHDF2 and MOB3B were obtained after dual luciferase reporter, ChIP, and PAR-CLIP assays. Me-RIP assay was used to determine m6A modification level of MOB3B mRNA in PCa cells. Mouse xenograft models of PCa cells were also established to monitor the tumor growth.

resultsKDM5A was highly expressed in human PCa tissues and cell lines. Upregulated KDM5A stimulated PCa cell proliferation, migration and invasion, but reduced cell apoptosis. Mechanistically, KDM5A, as a H3K4me3 demethylase, bound to the miR-495 promoter, which led to inhibition of its transcription and expression. As a target of miR-495, YTHDF2 could inhibit MOB3B expression by recognizing m6A modification of MOB3B mRNA and inducing mRNA degradation. Furthermore, KDM5A was found to downregulate MOB3B expression, consequently augmenting PCa cell proliferation, migration and invasion in vitro and promoting tumor growth in vivo via the miR-495/YTHDF2 axis.

conclusionIn summary, our study highlights the potential of histone demethylase KDM5A activity in enhancing PCa progression, and suggests KDM5A as a promising target for PCa treatment.

Indexed as

Gene Expression Regulation, NeoplasticAdenosineAnimalsApoptosisBiomarkers, TumorCell MovementCell ProliferationDisease ProgressionHumansMaleMiceMice, Inbred BALB CMice, NudeMicroRNAsMicrotubule-Associated ProteinsPrognosisAdenosineBiomarkers, TumorKDM5A protein, humanMicroRNAsMicrotubule-Associated ProteinsMIRN495 microRNA, humanMOB3B protein, humanN-methyladenosineRetinoblastoma-Binding Protein 2RNA-Binding ProteinsYTHDF2 protein, humanInvasionKDM5Am6A modificationmicroRNA-145MigrationMOB3BProstate cancerYTHDF2

Identifiers

PMID33087165
PMCPMC7576758
OpenAlexW3094083846

What Socratic 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 Socratic graph.