Evidence map›Paper›PMID 32269209›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2020

Upregulation of Neural Cell Adhesion Molecule 1 (NCAM1) by hsa-miR-141-3p Suppresses Ameloblastoma Cell Migration.

Gengyao Guan, Xing Niu, Xue Qiao, Xiaobin Wang, Jinwen Liu, Ming Zhong

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

Article in Medical science monitor : international medical journal of experimental and clinical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
6.2field-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

23 citing papers in PubMed, 46 citations in OpenAlex.

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  14. Analysis of miRNAs inPharmaceuticals (Basel, Switzerland) · 2023
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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

6 authors at 1 institution in 1 country.

Gengyao GuanDepartment of Oral Histopathology, School and Hospital of Stomatology, China Medical University, Liaoning Province Key Laboratory of Oral Disease, Shenyang, Liaoning, China (mainland).
Xing NiuDepartment of Oral Histopathology, School and Hospital of Stomatology, China Medical University, Liaoning Province Key Laboratory of Oral Disease, Shenyang, Liaoning, China (mainland).
Xue QiaoCentral Laboratory Department, School and Hospital of Stomatology, China Medical University, Liaoning Province Key Laboratory of Oral Disease, Shenyang, Liaoning, China (mainland).
Xiaobin WangDepartment of Oral Histopathology, School and Hospital of Stomatology, China Medical University, Liaoning Province Key Laboratory of Oral Disease, Shenyang, Liaoning, China (mainland).
Jinwen LiuDepartment of Oral Histopathology, School and Hospital of Stomatology, China Medical University, Liaoning Province Key Laboratory of Oral Disease, Shenyang, Liaoning, China (mainland).
Ming ZhongDepartment of Oral Histopathology, School and Hospital of Stomatology, China Medical University, Liaoning Province Key Laboratory of Oral Disease, Shenyang, Liaoning, China (mainland).
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Neural cell adhesion molecule 1 (NCAM1; CD56) and E-cadherin are both involved in cell-cell adhesion and cell development processes, and their dysregulation is associated with various tumors. We hypothesized that dysregulated NCAM1 could suppress the invasive behavior of ameloblastoma (AB), and its expression was regulated by miR-141-3p. MATERIAL AND METHODS Real-time qPCR was performed to examine differences in miR-141-3p expression between AB tissues and normal oral tissues (NOMs). The potential target NCAM1 of miR-141-3p was predicted by bioinformatics analysis, which was validated through dual-luciferase assay. The mRNA and protein levels of NCAM1 were detected by real-time qPCR and Western blot, respectively. Furthermore, the expression and distribution of NCAM1 in AB were investigated through immunohistochemical staining, and immunohistochemical staining of E-cadherin was also performed. After overexpression of NCAM1, the migration of AM-1 cells was examined using wound-healing assay. RESULTS Real-time qPCR results confirmed that miR-141-3p was significantly downregulated in AB tissues. According to bioinformatics analysis, NCAM1 was a target of miR-141-3p, which was confirmed by dual luciferase assay. We found that NCAM1 was significantly upregulated in AB tissues at the mRNA and protein levels. Furthermore, NCAM1 and E-cadherin were mainly expressed on the cell membrane of AB. Downregulation of E-cadherin was found in AB tissues. As shown in wound-healing assay results, NCAM1 overexpression significantly inhibited the invasiveness of AM-1 cells. CONCLUSIONS In this study, highly expressed NCAM1 was found in AB, and it suppressed the migration of AB cells and was regulated by miR-141-3p, suggesting its potential value as a therapeutic target for AB.

Indexed as

AdultAgedAged, 80 and overAmeloblastomaCD56 AntigenCell MovementCell ProliferationFemaleHumansJaw NeoplasmsMaleMicroRNAsMiddle AgedSignal TransductionTranscriptional ActivationUp-RegulationCD56 AntigenMicroRNAsMIRN141 microRNA, humanNCAM1 protein, human

Identifiers

PMID32269209
PMCPMC7169440
OpenAlexW3014209105

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.