Evidence map›Paper›PMID 38169586›Full record

ArticleInternational journal of medical sciences2024

LINC00662 promotes melanoma progression by competitively binding miR-107 and activating the β-catenin signaling pathway.

Mengmeng Luo, Rui Lei, Qingfang Zhao, Yichen Shen, Zhigang He, Jinghong Xu

Open access · goldAbstract read
In one paragraph

Article in International journal of medical sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-weighted citation impact, top 16% 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

7 citing papers in PubMed, 6 citations in OpenAlex.

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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 2 institutions in 1 country.

Mengmeng LuoDepartment of Plastic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University; Hangzhou, China.
Rui LeiDepartment of Plastic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University; Hangzhou, China.
Qingfang ZhaoDepartment of Plastic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University; Hangzhou, China.
Yichen ShenDepartment of Plastic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University; Hangzhou, China.
Zhigang HeDepartment of Plastic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University; Hangzhou, China.
Jinghong XuDepartment of Plastic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University; Hangzhou, China.
First Affiliated Hospital Zhejiang University · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Melanoma is a highly malignant tumor in the body. Long non-coding RNAs (lncRNAs) have been reported to be involved in the development of various tumors. Emerging evidence demonstrates the critical role of lncRNAs in melanoma development. In this study, we aimed to investigate the expression, biological function and regulatory mechanism of LINC00662 in melanomas. First, we found that LINC00662 was up-regulated in melanoma tissues and cell lines. High expression of LINC00662 in melanomas was associated with a poor patient prognosis. Silencing of LINC00662 suppressed the proliferation, migration, and invasion of melanoma cells

Indexed as

MelanomaMicroRNAsRNA, Long Noncodingbeta CateninCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansSignal Transductionbeta CateninMicroRNAsMIRN107 microRNA, humanRNA, Long NoncodingLINC00662MelanomaMiR-107POU3F2

Identifiers

PMID38169586
PMCPMC10758139
OpenAlexW4389340082

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.