Evidence map›Paper›PMID 32811869›Full record

ArticleScientific reports2020

LncRNA EIF3J-AS1 enhanced esophageal cancer invasion via regulating AKT1 expression through sponging miR-373-3p.

Wei-Tian Wei, Liang Wang, Jin-Xiao Liang, Jiang-Feng Wang, Qing Li, Jian Zeng

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Roles of long non-coding RNAs in oesophageal cancer pathogenesis.International journal of experimental pathology · 2025
    Review
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  15. Review
  16. Long non-coding RNAJournal of gastrointestinal oncology · 2021
    Article
  17. 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.

Wei-Tian WeiDepartment of Thoracic Surgery, Institute of Cancer Research and Basic Medical Sciences of Chinese Academy of Sciences, Cancer Hospital of University of Chinese Academy of Sciences, Zhejiang Cancer Hospital, No. 1 Banshan East Road, Gongshu District, Hangzhou, 310022, China.
Liang WangDepartment of Thoracic Surgery, Institute of Cancer Research and Basic Medical Sciences of Chinese Academy of Sciences, Cancer Hospital of University of Chinese Academy of Sciences, Zhejiang Cancer Hospital, No. 1 Banshan East Road, Gongshu District, Hangzhou, 310022, China.
Jin-Xiao LiangDepartment of Thoracic Surgery, Institute of Cancer Research and Basic Medical Sciences of Chinese Academy of Sciences, Cancer Hospital of University of Chinese Academy of Sciences, Zhejiang Cancer Hospital, No. 1 Banshan East Road, Gongshu District, Hangzhou, 310022, China.
Jiang-Feng WangDepartment of Thoracic Surgery, Institute of Cancer Research and Basic Medical Sciences of Chinese Academy of Sciences, Cancer Hospital of University of Chinese Academy of Sciences, Zhejiang Cancer Hospital, No. 1 Banshan East Road, Gongshu District, Hangzhou, 310022, China.
Qing LiDepartment of Thoracic Surgery, Institute of Cancer Research and Basic Medical Sciences of Chinese Academy of Sciences, Cancer Hospital of University of Chinese Academy of Sciences, Zhejiang Cancer Hospital, No. 1 Banshan East Road, Gongshu District, Hangzhou, 310022, China.
Jian ZengDepartment of Thoracic Surgery, Institute of Cancer Research and Basic Medical Sciences of Chinese Academy of Sciences, Cancer Hospital of University of Chinese Academy of Sciences, Zhejiang Cancer Hospital, No. 1 Banshan East Road, Gongshu District, Hangzhou, 310022, China. zengjian197877@163.com.
Cancer Hospital of Chinese Academy of Medical Sciences · CNUniversity of Chinese Academy of Sciences · CNZhejiang Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Esophageal cancer (ECa) remains a major cause of mortality across the globe. The expression of EIF3J-AS1 is altered in a plethora of tumors, but its role in ECa development and progression are undefined. Here, we show that EIF3J-AS1 is up-regulated in ECa and that its expression correlates with advanced TNM stage (P = 0.014), invasion depth (P = 0.001), positive lymph node metastasis (P < 0.001) and poor survival (OS: P = 0.0059; DFS: P = 0.0037) in ECa. Functional experiments showed that knockdown EIF3J-AS1 inhibited ECa growth and metastasis through in vitro and in vivo experiments. Regarding the mechanism, EIF3J-AS1/miR-373-3p/AKT1 established the ceRNA network involved in the modulation of cell progression of ECa cells. Overall, EIF3J-AS1 may exhibit an oncogenic function in ECa via acting as a sponge for miR-373-3p to up-regulate AKT1 mRNA level, and may serve as a potential therapeutic target and a prognostic biomarker for ECa patients.

Indexed as

AdultAgedAged, 80 and overApoptosisCarcinogenesisCell Line, TumorCell MovementCell ProliferationDisease ProgressionEsophageal NeoplasmsFemaleGene ExpressionHumansLymphatic MetastasisMaleMicroRNAsAKT1 protein, humanMicroRNAsMIRN373 microRNA, humanProto-Oncogene Proteins c-aktRNA, Long Noncoding

Identifiers

PMID32811869
PMCPMC7434778
OpenAlexW3054270643

What Socratic holds

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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 Socratic graph.