Evidence map›Paper›PMID 31371390›Full record

ArticleJournal of investigative medicine : the official publication of the American Federation for Clinical Research2020

lncRNA SLC16A1-AS1 as a novel prognostic biomarker in non-small cell lung cancer.

Hong Yue Liu, Sheng Rong Lu, Zi Han Guo, Zhi Sheng Zhang, Xuan Ye, Qiong Du, Huan Li, Qiang Wu, Bo Yu, Qing Zhai and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of investigative medicine : the official publication of the American Federation for Clinical Research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

33 citing papers in PubMed, 50 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

11 authors at 4 institutions in 1 country.

Hong Yue Liu *Department of Pharmacy, Fudan University Shanghai Cancer Center, Shanghai, China.
Sheng Rong Lu *Department of Pharmacy, The Central Hospital of Min-Hang District, Shanghai, China.
Zi Han Guo *Department of Pharmacy, Fudan University Shanghai Cancer Center, Shanghai, China.
Zhi Sheng Zhang *Department of Pharmacy, Fudan University Shanghai Cancer Center, Shanghai, China.
Xuan YeDepartment of Pharmacy, Fudan University Shanghai Cancer Center, Shanghai, China.
Qiong DuDepartment of Pharmacy, Fudan University Shanghai Cancer Center, Shanghai, China.
Huan LiDepartment of Pharmacy, Fudan University Shanghai Cancer Center, Shanghai, China.
Qiang WuDepartment of Oncology, The Second Affiliated Hospital of Anhui Medical University, Anhui, China.
Bo YuDepartment of Pharmacy, Fudan University Shanghai Cancer Center, Shanghai, China.
Qing ZhaiDepartment of Pharmacy, Fudan University Shanghai Cancer Center, Shanghai, China.
Jin Long LiuDepartment of Biotechnology and Pathology, School of Medical Technology, Shanghai University of Medicine & Health Sciences, Shanghai, China.ORCID 0000-0001-5574-6799
Shanghai Medical College of Fudan University · CNAnhui Medical University · CNMinhang District Central Hospital · CNShanghai University of Medicine and Health Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long non-coding RNAs (lncRNAs) have proved to act as crucial biomarkers in tumors. Novel biomarkers in non-small cell lung cancer (NSCLC) need to be investigated badly. To identify the differentially expressed lncRNAs between NSCLC tissue and adjacent tissue, microarray analysis was performed. lncRNA SLC16A1-AS1 was significantly less expressed in NSCLC tissue than that in adjacent tissue. Gain-of-function experiments was performed to determine the biological functions of SLC16A1-AS. In situhybridization and survival analysis were applied in lung cancer tissue samples to determine the prognostic role of SLC16A1-AS1. It was showed that SLC16A1-AS1 was remarkably downregulated in NSCLC tissues and cell lines. Functionally, SLC16A1-AS1 overexpression could inhibit the viability and proliferation of lung cancer cell, block the cell cycle and promote cell apoptosis in vitro which may result from reduced phosphorylation of rat sarcoma (RAS)/ proto-oncogene serine/threonine-protein kinase (RAF)/ mitogen-activated protein kinase kinase (MEK)/ extracellular regulated protein kinases (ERK) pathway caused by elevated expression of SLC16A1-AS1. Clinical sample analysis showed that SLC16A1-AS1 had a favorable impact on the overall survival and progression-free survival of patients with NSCLC. Our results suggested that SLC16A1-AS1 may act as a potential biomarker for patients with NSCLC.

Indexed as

Biomarkers, TumorCarcinoma, Non-Small-Cell LungCells, CulturedGene Expression ProfilingHumansLung NeoplasmsMicroarray AnalysisMonocarboxylate Transport Protein 1Monocarboxylic Acid TransportersPrognosisProto-Oncogene MasReal-Time Polymerase Chain ReactionRNA, Long NoncodingSurvival AnalysisSymportersBiomarkers, TumorMAS1 protein, humanMonocarboxylate Transport Protein 1Monocarboxylic Acid TransportersProto-Oncogene MasRNA, Long NoncodingSymportersnon-small cell lung cancerprognosisproliferationSLC16A1-AS1

Identifiers

PMID31371390
PMCPMC6996107
OpenAlexW2965573074

What OpenQuestion holds

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LicenceCC BY
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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.