Evidence map›Paper›PMID 38561355›Full record

ArticleCell death discovery2024

A novel long non-coding RNA SLNCR1 promotes proliferation, migration, and invasion of melanoma via transcriptionally regulating SOX5.

Lele Cong, Qing Zhao, Hongyan Sun, Zilong Zhou, Yue Hu, Chunyi Li, Miao Hao, Xianling Cong

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

Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.7field-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

9 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

8 authors at 3 institutions in 1 country.

Lele CongDepartment of Dermatology, China-Japan Union Hospital of Jilin University, Changchun, Jilin, China.
Qing ZhaoDepartment of Neurology, China-Japan Union Hospital of Jilin University, Changchun, Jilin, China.
Hongyan SunDepartment of Biobank, China-Japan Union Hospital of Jilin University, Changchun, Jilin, China.
Zilong ZhouDepartment of Biobank, China-Japan Union Hospital of Jilin University, Changchun, Jilin, China.
Yue HuDepartment of Biobank, China-Japan Union Hospital of Jilin University, Changchun, Jilin, China.
Chunyi LiInstitute of Antler Science and Product Technology, Changchun Sci-Tech University, Changchun, China.ORCID http://orcid.org/0000-0001-7275-4440
Miao HaoScientific Research Center, China-Japan Union Hospital of Jilin University, Changchun, Jilin, China. miaohao@jlu.edu.cn.ORCID http://orcid.org/0000-0002-8386-2145
Xianling CongDepartment of Biobank, China-Japan Union Hospital of Jilin University, Changchun, Jilin, China. congxl@jlu.edu.cn.
Jilin University · CNChangchun University · CNUnion Hospital · CN

Funding

Department of Science and Technology of Jilin Province (Jilin Province Science and Technology Department) 20230402003GHDepartment of Science and Technology of Jilin Province (Jilin Province Science and Technology Department) YDZJ202201ZYTS021
6 · The paper itself

Abstract

Steroid receptor RNA activator (SRA)-like non-coding RNA (SLNCR1) has been implicated in various tumorigenic processes, but the precise regulatory role in melanoma progression remains uncertain. We performed a comprehensive analysis to investigate the prognostic value of SLNCR1 expression in patients with melanoma by TCGA database and melanoma tissue samples via the Kaplan-Meier method. Subsequently, we conducted qRT-PCR and Fluorescence in Situ Hybridization (FISH) assays to identify SLNCR1 expression levels and localization in tissues and cells, respectively. Loss-of-function assays utilizing shRNAs vectors were used to investigate the potential impact of SLNCR1. Our data showed that SLNCR1 is significantly up-regulated in human malignant melanoma tissues and cell lines and functions as an oncogene. Silencing of SLNCR1 suppressed melanoma cell proliferation, migration, invasion, and inhibited tumorigenesis in a mouse xenograft model. Additionally, we employed bioinformatic predictive analysis, combined with dual-luciferase reporter analysis and functional rescue assays, to elucidate the mechanistic target of the SLNCR1/SOX5 axis in melanoma. Mechanistically, we discovered that SLNCR1 promotes EMT of human melanoma by targeting SOX5, as downregulation of SLNCR1 expression leads to a decrease in SOX5 protein levels and inhibits melanoma tumorigenesis. Our research offers promising insights for more precise diagnosis and treatment of human melanoma.

Identifiers

PMID38561355
PMCPMC10984963
OpenAlexW4393374646

What OpenQuestion holds

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Registered trials

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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.