Evidence map›Paper›PMID 32878637›Full record

ArticleGenome medicine2020

FOXC1-mediated LINC00301 facilitates tumor progression and triggers an immune-suppressing microenvironment in non-small cell lung cancer by regulating the HIF1α pathway.

Cheng-Cao Sun, Wei Zhu, Shu-Jun Li, Wei Hu, Jian Zhang, Yue Zhuo, Han Zhang, Juan Wang, Yu Zhang, Shao-Xin Huang and 2 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Genome medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 100 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed, 1 pooled it
12.2field-weighted citation impact, top 1% 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

100 citing papers in PubMed, 1 synthesis or guideline pooled it, 190 citations in OpenAlex.

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  18. Ultrasound-responsive BiJournal of nanobiotechnology · 2024
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40 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 2 countries.

Cheng-Cao Sun *Department of Preventive Medicine, School of Health Sciences, Wuhan University, No.115 Donghu Road, Wuchang District, Wuhan, 430071, Hubei, People's Republic of China. chengcaosun@whu.edu.cn.ORCID http://orcid.org/0000-0002-0554-3165
Wei Zhu *Department of Preventive Medicine, School of Health Sciences, Wuhan University, No.115 Donghu Road, Wuchang District, Wuhan, 430071, Hubei, People's Republic of China.
Shu-Jun Li *Wuhan Hospital for the Prevention and Treatment of Occupational Diseases, Wuhan, 430022, Hubei, People's Republic of China.
Wei HuDepartment of Preventive Medicine, School of Health Sciences, Wuhan University, No.115 Donghu Road, Wuchang District, Wuhan, 430071, Hubei, People's Republic of China.
Jian ZhangDepartment of Preventive Medicine, School of Health Sciences, Wuhan University, No.115 Donghu Road, Wuchang District, Wuhan, 430071, Hubei, People's Republic of China.
Yue ZhuoDepartment of Preventive Medicine, School of Health Sciences, Wuhan University, No.115 Donghu Road, Wuchang District, Wuhan, 430071, Hubei, People's Republic of China.
Han ZhangDepartment of Preventive Medicine, School of Health Sciences, Wuhan University, No.115 Donghu Road, Wuchang District, Wuhan, 430071, Hubei, People's Republic of China.
Juan WangDepartment of Preventive Medicine, School of Health Sciences, Wuhan University, No.115 Donghu Road, Wuchang District, Wuhan, 430071, Hubei, People's Republic of China.
Yu ZhangDepartment of Preventive Medicine, School of Health Sciences, Wuhan University, No.115 Donghu Road, Wuchang District, Wuhan, 430071, Hubei, People's Republic of China.
Shao-Xin HuangSchool of Basic Medicine, Jiujiang University, Jiujiang, 332005, Jiangxi, People's Republic of China.
Qi-Qiang HeDepartment of Preventive Medicine, School of Health Sciences, Wuhan University, No.115 Donghu Road, Wuchang District, Wuhan, 430071, Hubei, People's Republic of China. heqiqiang@gmail.com.
De-Jia LiDepartment of Preventive Medicine, School of Health Sciences, Wuhan University, No.115 Donghu Road, Wuchang District, Wuhan, 430071, Hubei, People's Republic of China. lodjlwhu@sina.com.
Wuhan University · CNJiujiang University · CNThe University of Texas MD Anderson Cancer Center · USWuhan Prevention and Treatment Center for Occupational Diseases · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLong non-coding RNAs (lncRNAs) are extensively intricate in the tumorigenesis and metastasis of various cancer types. Nevertheless, the detailed molecular mechanisms of lncRNA in non-small cell lung cancer (NSCLC) still remain mainly undetermined.

methodsqPCR was performed to verify LINC00301 expression in NSCLC clinical specimens or cell lines. Fluorescence in situ hybridization (FISH) was conducted to identify the localization of LINC00301 in NSCLC cells. Chromatin immunoprecipitation (ChIP) was subjected to validate the binding activity between FOXC1 and LINC00301 promoters. RNA immunoprecipitation (RIP) was performed to explore the binding activity between LINC00301 and EZH2. RNA pull-down followed by dot-blot, protein domain mapping, and RNA electrophoresis mobility shift assay (EMSA) were conducted to identify the detailed binding regions between LINC00301 and EZH2. Alpha assay was conducted to quantitatively assess the interaction between LINC00301 and EZH2.

resultsLINC00301 is highly expressed in NSCLC and closely corelated to its prognosis by analyzing the relationship between differentially expressed lncRNAs and prognosis in NSCLC samples. in vitro and in vivo experiments revealed that LINC00301 facilitates cell proliferation, releases NSCLC cell cycle arrest, promotes cell migration and invasion, and suppresses cell apoptosis in NSCLC. In addition, LINC00301 increases regulatory T cell (Treg) while decreases CD8

conclusionsIn summary, our present research revealed the oncogenic roles of LINC00301 in clinical specimens as well as cellular and animal experiments, illustrating the potential roles and mechanisms of the FOXC1/LINC00301/EZH2/EAF2/pVHL/HIF1α and FOXC1/LINC00301/miR-1276/HIF1α pathways, which provides novel insights and potential theraputic targets to NSCLC.

Indexed as

AnimalsBinding SitesCarcinoma, Non-Small-Cell LungCell CycleCell Line, TumorDisease Models, AnimalDisease ProgressionDNA MethylationForkhead Transcription FactorsGene Expression Regulation, NeoplasticHistonesHumansHypoxia-Inducible Factor 1, alpha SubunitImmunomodulationLung NeoplasmsMiceForkhead Transcription FactorsFOXC1 protein, humanHIF1A protein, humanHistonesHypoxia-Inducible Factor 1, alpha SubunitRNA, Long NoncodingELL protein-associated factor 2 (EAF2)Enhancer of zeste homolog 2 (EZH2)Hypoxia-inducible factor 1 α (HIF1α)LINC00301miR-1276Non-small cell lung cancer (NSCLC)Regulatory T cells (Treg)Tumorigenesis

Identifiers

PMID32878637
PMCPMC7466809
OpenAlexW4244055564

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.