Evidence map›Paper›PMID 36494339›Full record

ArticleCell death discovery2022

Gene amplification-driven lncRNA SNHG6 promotes tumorigenesis via epigenetically suppressing p27 expression and regulating cell cycle in non-small cell lung cancer.

Qi Wang, Wei Zhang, Dandan Yin, Zaibin Tang, Erbao Zhang, Weibing Wu

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
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  9. LncRNA CALML3-AS1 modulated by mCancer gene therapy · 2023
    Article
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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 3 institutions in 1 country.

Qi Wang *Department of Thoracic Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.ORCID http://orcid.org/0000-0002-3035-5887
Wei Zhang *Department of Thoracic Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Dandan Yin *Clinical Research Center, The Second Hospital of Nanjing, Nanjing University of Chinese Medicine, Zhong Fu Road, Gulou District, Nanjing, Jiangsu, 210003, PR China.
Zaibin TangDepartment of Thoracic Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Erbao ZhangDepartment of Epidemiology, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, China. erbaozhang@njmu.edu.cn.ORCID http://orcid.org/0000-0002-5752-7976
Weibing WuDepartment of Thoracic Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China. wuweibing95@126.com.ORCID http://orcid.org/0000-0001-7306-1515
Jiangsu Province Hospital · CNJiangsu Cancer Hospital · CNNanjing University of Chinese Medicine · CN

Funding

Ministry of Health of China | Wu Jieping Medical Foundation 320.2730.1868Natural Science Foundation of Jiangsu Province (Jiangsu Provincial Natural Science Foundation) BK20211253Six Talent Peaks Project in Jiangsu Province (Six Talent Peaks Project in Jiangsu Province of China) WSW-007
6 · The paper itself

Abstract

Long non-coding RNAs (lncRNAs) have been validated to play essential roles in non-small cell lung carcinoma (NSCLC) progression. In this study, through systematically screening GSE33532 and GSE29249 from Gene Expression Omnibus (GEO) database and bioinformatics analysis, we found the significant upregulation of SNHG6 in NSCLC. The activation of SNHG6 was driven by copy number amplification and high expression of SNHG6 indicated a poor prognosis. Functionally, the knockdown of SNHG6 inhibited NSCLC cell proliferation, migration, and suppressed the G1/S transition of the cell cycle. SNHG6 overexpression had the opposite effects. Mechanically, SNHG6 recruited EZH2 to the promoter region of p27 and increased H3K27me3 enrichment, thus epigenetically repressing the expression of p27, regulating the cell cycle, and promoting tumorigenesis of NSCLC. SNHG6 silencing restrained tumor growth in vivo and suppressed the expressions of cell cycle-related proteins in the G1/S transition. In conclusion, our study uncovered a novel mechanism of SNHG6 activation and its function. SNHG6 can be considered a potential target for the diagnosis and treatment of NSCLC in the future.

Identifiers

PMID36494339
PMCPMC9734177
OpenAlexW4311289500

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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.