Evidence map›Paper›PMID 33308223›Full record

ArticleMolecular cancer2020

Long non-coding RNA NEAT1 promotes bone metastasis of prostate cancer through N6-methyladenosine.

Simeng Wen, Yulei Wei, Chong Zen, Wei Xiong, Yuanjie Niu, Yu Zhao

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 173 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
173citing papers in PubMed, 4 pooled it
16.3field-weighted citation impact, top 1% 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

173 citing papers in PubMed, 4 syntheses or guidelines pooled it, 271 citations in OpenAlex.

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113 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

6 authors at 4 institutions in 2 countries.

Simeng WenDepartment of Urology, The Second Hospital of Tianjin Medical University, Tianjin Medical University, Tianjin, 300211, China.
Yulei WeiDepartment of Gynecology and Obstetrics, Tianjin First Central Hospital, Tianjin, 300192, China.
Chong ZenDepartment of Urology, Central South University, Changsha, 410011, China.
Wei XiongDepartment of Urology, Central South University, Changsha, 410011, China.
Yuanjie NiuDepartment of Urology, The Second Hospital of Tianjin Medical University, Tianjin Medical University, Tianjin, 300211, China. niuyuanjie@tmu.edu.cn.
Yu ZhaoDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN, 55905, USA. zhao.yu@mayo.edu.ORCID 0000-0002-1242-2257
Central South University · CNSecond Hospital of Tianjin Medical University · CNMayo Clinic · USTianjin First Center Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundN6-methyladenosine (m6A) is the most prevalent messenger RNA modification in mammalian cells. However, the disease relevant function of m6A on specific oncogenic long non-coding RNAs (ncRNAs) is not well understood.

methodsWe analyzed the m6A status using patients samples and bone metastatic PDXs. Through m6A high-throughput sequencing, we identified the m6A sites on NEAT1-1 in prostate bone metastatic PDXs. Mass spec assay showed interaction among NEAT1-1, CYCLINL1 and CDK19. RNA EMSA, RNA pull-down, mutagenesis, CLIP, western blot, ChIP and ChIRP assays were used to investigate the molecular mechanisms underlying the functions of m6A on NEAT1-1. Loss-of function and rescued experiments were executed to detect the biological roles of m6A on NEAT1-1 in the PDX cell phenotypes in vivo.

resultsIn this study, we identified 4 credible m6A sites on long ncRNA NEAT1-1. High m6A level of NEAT1-1 was related to bone metastasis of prostate cancer and m6A level of NEAT1-1 was a powerful predictor of eventual death. Transcribed NEAT1-1 served as a bridge to facility the binding between CYCLINL1 and CDK19 and promoted the Pol II ser2 phosphorylation. Importantly, depletion of NEAT1-1or decreased m6A of NEAT1-1 impaired Pol II Ser-2p level in the promoter of RUNX2. Overexpression of NEAT1-1 induced cancer cell metastasis to lung and bone; xenograft growth and shortened the survival of mice, but NEAT1-1 with m6A site mutation failed to do these.

conclusionCollectively, the findings indicate that m6A on ncRNA NEAT1-1 takes critical role in regulating Pol II ser2 phosphorylation and may be novel specific target for bone metastasis cancer therapy and diagnosis. New complex CYCLINL1/CDK19/NEAT1-1 might provide new insight into the potential mechanism of the pathogenesis and development of bone metastatic prostate cancer.

Indexed as

AdenosineAgedAged, 80 and overAnimalsBone NeoplasmsCell Line, TumorCore Binding Factor Alpha 1 SubunitCyclin-Dependent KinasesCyclinsHumansMaleMice, NudeMiddle AgedPhosphorylationPhosphoserinePrognosisAdenosineCCNL1 protein, humanCDK19 protein, humanCore Binding Factor Alpha 1 SubunitCyclin-Dependent KinasesCyclinsNEAT1 long non-coding RNA, humanN-methyladenosinePhosphoserineRNA, Long NoncodingRNA Polymerase IIBone metastatic prostate cancerCDK19CYCLINL1m6AncRNANEAT1–1

Identifiers

PMID33308223
PMCPMC7733260
OpenAlexW3112762656

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.