Evidence map›Paper›PMID 32193153›Full record

ArticleMolecular therapy. Nucleic acids2020

MCM3AP-AS1 KD Inhibits Proliferation, Invasion, and Migration of PCa Cells via DNMT1/DNMT3 (A/B) Methylation-Mediated Upregulation of NPY1R.

Xin Li, Jiancheng Lv, Shuai Liu

RetractedErratum issuedOpen access · goldAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular therapy. Nucleic acids, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 12% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
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  10. MCM3AP-AS1: An Indispensable Cancer-Related LncRNA.Frontiers in cell and developmental biology · 2021
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 2 countries.

Xin LiDepartment of Urology, Shandong Provincial Hospital Affiliated to Shandong University, Ji'nan 250021, P. R. China; Department of Urology, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan.
Jiancheng LvDepartment of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, P. R. China.
Shuai LiuDepartment of Urology, Shandong Provincial Hospital Affiliated to Shandong University, Ji'nan 250021, P. R. China. Electronic address: 15866600623@163.com.
Nanjing Medical University · CNShandong Provincial Hospital · CNShandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer (PCa) is a heterogeneous tumor that commonly occurs among males worldwide. This study explored the potential role that long non-coding RNA MCM3AP antisense RNA 1 (MCM3AP-AS1) plays in PCa progression, and investigated its mechanism. MCM3AP-AS1 and neuropeptide Y receptor Y1 (NPY1R) expression was determined in PCa cells. The regulatory role of MCM3AP-AS1 in PCa cells was defined using scratch test, Transwell assay, 5-ethynyl-2'-deoxyuridine (EdU) assay, and flow cytometry. Methylation-specific PCR (MSP) was used to test the methylation level of NPY1R. Subsequently, the interaction among MCM3AP-AS1, DNA methyltransferase (DNMT)1/DNMT3 (A/B), and NPY1R was investigated using RNA immunoprecipitation, RNA pull-down, and chromatin immunoprecipitation. Finally, we observed xenograft tumor in nude mice. MCM3AP-AS1 was highly, whereas NPY1R was poorly, expressed in PCa. Lentivirus-mediated overexpression of MCM3AP-AS1 promoted proliferation, invasion, and migration while suppressing apoptosis of PCa cells, whereas opposite trends were detected after inhibition of the mitogen-activated protein kinase (MAPK) pathway. MCM3AP-AS1 promoted methylation of NPY1R promoter via recruitment of DNMT1/DNMT3 (A/B), thereby downregulating NPY1R expression to activate the MAPK pathway. Furthermore, overexpressed MCM3AP-AS1 was observed to facilitate PCa development in vivo, which could be reversed by overexpressed NPY1R. Altogether, MCM3AP-AS1 silencing inhibits PCa progression by disrupting methylation of the NPY1R promoter to inactivate the MAPK pathway.

Indexed as

apoptosisDNA methyltransferaseinvasionlong non-coding RNA MCM3AP-AS1MAPK pathwaymigrationneuropeptide Y receptor Y1proliferationprostate cancerxenograft in nude mice

Identifiers

PMID32193153
PMCPMC7078492
OpenAlexW3002425391

What Socratic 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 Socratic graph.