Evidence map›Paper›PMID 32130660›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2020

Long noncoding RNA LINC01234 silencing exerts an anti-oncogenic effect in esophageal cancer cells through microRNA-193a-5p-mediated CCNE1 downregulation.

Jun Ma, Li-Na Han, Jian-Rui Song, Xiao-Ming Bai, Ju-Zi Wang, Li-Feng Meng, Jian Li, Wen Zhou, Yun Feng, Wei-Rong Feng and 3 more

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 30 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

13 authors at 3 institutions in 2 countries.

Jun MaDepartment of Thoracic Surgery, Shanxi Provincial People's Hospital, No. 29, Shuangta Temple Street, Taiyuan, 030012, Shanxi Province, People's Republic of China. Drjunma789@163.com.
Li-Na HanMedical Department, Shanxi Provincial People's Hospital, Taiyuan, 030012, People's Republic of China.
Jian-Rui SongDepartment of Cell and Developmental Biology, Department of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI, 48109, USA.
Xiao-Ming BaiDepartment of Thoracic Surgery, Shanxi Provincial People's Hospital, No. 29, Shuangta Temple Street, Taiyuan, 030012, Shanxi Province, People's Republic of China.
Ju-Zi WangDepartment of Thoracic Surgery, Shanxi Provincial People's Hospital, No. 29, Shuangta Temple Street, Taiyuan, 030012, Shanxi Province, People's Republic of China.
Li-Feng MengDepartment of Thoracic Surgery, Shanxi Provincial People's Hospital, No. 29, Shuangta Temple Street, Taiyuan, 030012, Shanxi Province, People's Republic of China.
Jian LiDepartment of Thoracic Surgery, Shanxi Provincial People's Hospital, No. 29, Shuangta Temple Street, Taiyuan, 030012, Shanxi Province, People's Republic of China.
Wen ZhouDepartment of Thoracic Surgery, Shanxi Provincial People's Hospital, No. 29, Shuangta Temple Street, Taiyuan, 030012, Shanxi Province, People's Republic of China.
Yun FengDepartment of Thoracic Surgery, Shanxi Provincial People's Hospital, No. 29, Shuangta Temple Street, Taiyuan, 030012, Shanxi Province, People's Republic of China.
Wei-Rong FengDepartment of Thoracic Surgery, Shanxi Provincial People's Hospital, No. 29, Shuangta Temple Street, Taiyuan, 030012, Shanxi Province, People's Republic of China.
Jun-Jun MaDepartment of Thoracic Surgery, Shanxi Provincial People's Hospital, No. 29, Shuangta Temple Street, Taiyuan, 030012, Shanxi Province, People's Republic of China.
Jun-Tao HaoDepartment of Thoracic Surgery, Shanxi Provincial People's Hospital, No. 29, Shuangta Temple Street, Taiyuan, 030012, Shanxi Province, People's Republic of China.
Zeng-Qiang ShenDepartment of Thoracic Surgery, Shanxi Provincial People's Hospital, No. 29, Shuangta Temple Street, Taiyuan, 030012, Shanxi Province, People's Republic of China.
Shaanxi Provincial People's Hospital · CNShanxi Medical University · CNUniversity of Michigan–Ann Arbor · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLong non-coding RNAs (lncRNAs) are transcribed pervasively in the genome and act to regulate chromatin remodeling and gene expression. Dysregulated lncRNA expression has been reported in many cancers, but the role of lncRNAs in esophageal cancer (EC) has so far remained poorly understood. In this study, we aimed to understand the effect of lncRNA LINC01234 on EC development through competitively binding to microRNA-193a-5p (miR-193a-5p).

methodsThe Gene Expression Omnibus (GEO) database was used for microarray-based EC expression profiling. Gain- and loss-of-function analyses were carried out in human EC-derived Eca-109 and EC9706 cells. Expression analyses of miR-193a-5p, LINC01234, CCNE1, caspase-3, p21, Bax, cyclinD1 and Bcl-2 were performed using RT-qPCR and Western blotting. Cell proliferation, colony formation and apoptosis analyses were carried out using MTT, Hoechst 33258 and flow cytometry assays. A xenograft EC model in nude mice was used to evaluate in vivo tumor growth and CCNE1 expression.

resultsMicroarray-based analyses revealed that LINC01234 expression was increased in primary EC samples, whereas that of miR-193a-5p was decreased. We found that CCNE1 was a target of miR-193a-5p and that LINC01234, in turn, sponges miR-193a-5p. After treatment with si-LINC01234 or miR-193a-5p mimic, EC cells (Eca-109 and EC9706) exhibited cyclinD1 and Bcl-2 downregulation, and caspase-3, p21, Bax and cleaved caspase-3 upregulation. LINC01234 silencing or miR-193a-5p upregulation resulted in decreased proliferation and colony formation, and increased apoptosis of EC cells. In addition, LINC01234 silencing or miR-193a-5p upregulation resulted in reduced in vivo EC tumor growth and CCNE1 expression in nude mice.

conclusionsWe found that silencing of LINC01234 suppresses EC development by inhibiting CCNE1 through competitively binding to miR-193a-5p, which suggests that LINC01234 may represent a novel target for EC therapy.

Indexed as

Gene Expression Regulation, NeoplasticGene SilencingAnimalsApoptosisCell Line, TumorCell ProliferationCyclin EDown-RegulationEsophageal NeoplasmsHumansMice, NudeMicroRNAsModels, BiologicalOncogene ProteinsRNA, Long NoncodingUp-RegulationCCNE1 protein, humanCyclin EMicroRNAsMIRN193 microRNA, humanOncogene ProteinsRNA, Long NoncodingApoptosisCCNE1Esophageal cancerLong noncoding RNA LINC01234microRNA-193a-5pProliferation

Identifiers

PMID32130660
PMCPMC12990743
OpenAlexW3009496449

What OpenQuestion holds

Textmetadata
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.