Evidence map›Paper›PMID 37647111›Full record

ArticleMolecular cancer research : MCR2023

m6A-Mediated Biogenesis of circDDIT4 Inhibits Prostate Cancer Progression by Sequestrating ELAVL1/HuR.

Zhe Kong, Yali Lu, Yue Yang, Kun Chang, Yan Lin, Yan Huang, Chenji Wang, Lu Zhang, Wei Xu, Shimin Zhao and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

21 citing papers in PubMed, 26 citations in OpenAlex.

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  18. Role of NOncology reports · 2024
    Review
  19. Non-coding RNA-Mediated N6-Methyladenosine (mNon-coding RNA research · 2024
    Review
  20. Review
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

11 authors at 2 institutions in 1 country.

Zhe Kong *Obstetrics and Gynecology Hospital of Fudan University, State Key Lab of Genetic Engineering, MOE Engineering Research Center of Gene Technology, School of Life Sciences, Key Laboratory of Reproduction Regulation of NPFPC (SIPPR, IRD), Fudan University, Shanghai, P.R. China.ORCID 0000-0001-7430-534X
Yali Lu *Obstetrics and Gynecology Hospital of Fudan University, State Key Lab of Genetic Engineering, MOE Engineering Research Center of Gene Technology, School of Life Sciences, Key Laboratory of Reproduction Regulation of NPFPC (SIPPR, IRD), Fudan University, Shanghai, P.R. China.ORCID 0000-0002-7487-0100
Yue Yang *Obstetrics and Gynecology Hospital of Fudan University, State Key Lab of Genetic Engineering, MOE Engineering Research Center of Gene Technology, School of Life Sciences, Key Laboratory of Reproduction Regulation of NPFPC (SIPPR, IRD), Fudan University, Shanghai, P.R. China.ORCID 0009-0000-9809-0283
Kun ChangDepartment of Urology, Fudan University Shanghai Cancer Center, Shanghai, P.R. China.ORCID 0000-0002-0126-197X
Yan LinInstitutes of Biomedical Sciences, Fudan University, Shanghai, P.R. China.ORCID 0009-0008-7960-7740
Yan HuangObstetrics and Gynecology Hospital of Fudan University, State Key Lab of Genetic Engineering, MOE Engineering Research Center of Gene Technology, School of Life Sciences, Key Laboratory of Reproduction Regulation of NPFPC (SIPPR, IRD), Fudan University, Shanghai, P.R. China.ORCID 0009-0000-1122-4761
Chenji WangObstetrics and Gynecology Hospital of Fudan University, State Key Lab of Genetic Engineering, MOE Engineering Research Center of Gene Technology, School of Life Sciences, Key Laboratory of Reproduction Regulation of NPFPC (SIPPR, IRD), Fudan University, Shanghai, P.R. China.ORCID 0000-0002-5752-6439
Lu ZhangObstetrics and Gynecology Hospital of Fudan University, State Key Lab of Genetic Engineering, MOE Engineering Research Center of Gene Technology, School of Life Sciences, Key Laboratory of Reproduction Regulation of NPFPC (SIPPR, IRD), Fudan University, Shanghai, P.R. China.ORCID 0000-0002-4858-0361
Wei XuInstitutes of Biomedical Sciences, Fudan University, Shanghai, P.R. China.ORCID 0000-0002-9858-589X
Shimin ZhaoObstetrics and Gynecology Hospital of Fudan University, State Key Lab of Genetic Engineering, MOE Engineering Research Center of Gene Technology, School of Life Sciences, Key Laboratory of Reproduction Regulation of NPFPC (SIPPR, IRD), Fudan University, Shanghai, P.R. China.ORCID 0000-0002-3674-9107
Yao LiObstetrics and Gynecology Hospital of Fudan University, State Key Lab of Genetic Engineering, MOE Engineering Research Center of Gene Technology, School of Life Sciences, Key Laboratory of Reproduction Regulation of NPFPC (SIPPR, IRD), Fudan University, Shanghai, P.R. China.ORCID 0000-0001-5257-7272
Fudan University · CNShanghai Medical College of Fudan University · CN

Funding

National Key Research and Development Program of China (NKPs) 2018YFA0800300National Key Research and Development Program of China (NKPs) 2018YFA0801300National Natural Science Foundation of China (NSFC) 31821002National Natural Science Foundation of China (NSFC) 31871432National Natural Science Foundation of China (NSFC) 31930062Shanghai Science and Technology Development Foundation (Shanghai Science and Technology Foundation) 20ZR1404500
6 · The paper itself

Abstract

The pathologic significance of the circular RNA DDIT4 (circDDIT4), which is formed by backsplicing at the 3'-untranslated region (UTR) with a 5' splice acceptor site in exon 2 of linear DDIT4 mRNA, has yet to be determined. Our study found that circDDIT4 is downregulated in prostate cancer and functions as a tumor suppressor during prostate cancer progression. By competitively binding to ELAV-like RNA binding protein 1 (ELAVL1/HuR) through its 3'-UTR, circDDIT4 acts as a protein sponge to decrease the expression of prostate cancer-overexpressed anoctamin 7 (ANO7). This promotes prostate cancer cell apoptosis while inhibiting cell proliferation and metastasis. Furthermore, we discovered that N6-methyladenosine (m6A) modification facilitates the biogenesis of circDDIT4. The methyltransferase complex consisting of WTAP/METTL3/METTL14 increases the level of circDDIT4, while the RNA demethylase FTO decreases it. IMPLICATIONS: These findings suggest that abnormal cotranscriptional modification of m6A promotes prostate cancer initiation and progression via a circular RNA-protein-cell signaling network.

Indexed as

Prostatic NeoplasmsRNA, CircularAlpha-Ketoglutarate-Dependent Dioxygenase FTOELAV-Like Protein 1HumansMaleMethyltransferasesRNA-Binding ProteinsSignal TransductionAlpha-Ketoglutarate-Dependent Dioxygenase FTOELAVL1 protein, humanELAV-Like Protein 1FTO protein, humanMethyltransferasesMETTL3 protein, humanRNA-Binding ProteinsRNA, Circular

Identifiers

PMID37647111
PMCPMC10690048
OpenAlexW4386271950

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.