Evidence map›Paper›PMID 26840083›Full record

ArticleOncotarget2016

Long non-coding RNA LINC01133 represses KLF2, P21 and E-cadherin transcription through binding with EZH2, LSD1 in non small cell lung cancer.

Chongshuang Zang, Feng-Qi Nie, Qian Wang, Ming Sun, Wei Li, Jing He, Meiling Zhang, Kai-Hua Lu

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 2 pooled it
6.9field-weighted citation impact, top 2% 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

62 citing papers in PubMed, 2 syntheses or guidelines pooled it, 96 citations in OpenAlex.

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  14. A review on the role of LINC01133 in cancers.Cancer cell international · 2022
    Review
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2 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Chongshuang ZangDepartment of Oncology, First Affiliated Hospital, Nanjing Medical University, Nanjing, People's Republic of China.
Feng-Qi NieDepartment of Oncology, Second Affiliated Hospital, Nanjing Medical University, Nanjing, People's Republic of China.
Qian WangDepartment of Oncology, First Affiliated Hospital, Nanjing Medical University, Nanjing, People's Republic of China.
Ming SunDepartment of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, People's Republic of China.
Wei LiDepartment of Oncology, First Affiliated Hospital, Nanjing Medical University, Nanjing, People's Republic of China.
Jing HeDepartment of Oncology, First Affiliated Hospital, Nanjing Medical University, Nanjing, People's Republic of China.
Meiling ZhangDepartment of Oncology, First Affiliated Hospital, Nanjing Medical University, Nanjing, People's Republic of China.
Kai-Hua LuDepartment of Oncology, First Affiliated Hospital, Nanjing Medical University, Nanjing, People's Republic of China.
Nanjing Medical University · CNSecond Affiliated Hospital of Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long non-coding RNAs are emerging as crucial regulators and prognostic markers in multiple cancers including non small cell lung cancer (NSCLC). In this study, we screened LINCO1133 as a new candidate lncRNA which promotes NSCLC development and progression, in two independent datasets (GSE18842 and GSE19804) from the Gene Expression Omnibus (GEO). LINC01133 is previously found to be over-expressed in lung squamous cell cancer (LSCC) and knockdown its expression inhibits LSCC cells invasion. However, its' molecular mechanism and downstream targets involving in regulation of cancer cells phenotype is not known. Here, we found that LINC01133 expression is up-regulated in NSCLC tissues, and its' over-expression is associated with patients poor prognosis and short survival time. LINC01133 knockdown decreased NSCLC cells proliferation, migration, invasion and induced cell cycle G1/S phase arrest and cell apoptosis. Mechanistic investigations showed that LINC01133 could interact with EZH2, LSD1 and recruit them to KLF2, P21 or E-cadherin promoter regions to repress their transcription. Furthermore, rescue experiments demonstrated that LINC01133 oncogenic function is partly through regulating KLF2. Lastly, we found that there was negative correlation between LINC01133 and KLF2, P21 or E-cadherin in NSCLC. Overall, our findings illuminate how LINC01133 over-expression confers an oncogenic function in NSCLC that may offer a novel therapy target in this disease.

Indexed as

A549 CellsAgedAnimalsAntigens, CDCadherinsCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationCyclin-Dependent Kinase Inhibitor p21Enhancer of Zeste Homolog 2 ProteinHeterograftsHistone DemethylasesHumansKruppel-Like Transcription FactorsLung NeoplasmsMiceAntigens, CDCadherinsCDH1 protein, humanCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21Enhancer of Zeste Homolog 2 ProteinEZH2 protein, humanHistone DemethylasesKDM1A protein, humanKLF2 protein, humanKruppel-Like Transcription Factorslong non-coding RNA LINC01133, humanRNA, Long NoncodingEZH2lncRNALSD1NSCLCproliferation

Identifiers

PMID26840083
PMCPMC4905504
OpenAlexW2291457701

What OpenQuestion holds

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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.