Evidence map›Paper›PMID 31920462›Full record

ArticleCancer cell international2020

Long non-coding RNA TUG1 promotes cell progression in hepatocellular carcinoma via regulating miR-216b-5p/DLX2 axis.

Qun Dai, Jingyi Deng, Jinrong Zhou, Zhuhong Wang, Xiao-Feng Yuan, Shunwen Pan, Hong-Bin Zhang

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.0field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 42 citations in OpenAlex.

  1. Deciphering the role ofWorld journal of hepatology · 2025
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  14. Role of long noncoding RNA taurine-upregulated gene 1 in cancers.Molecular medicine (Cambridge, Mass.) · 2021
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  17. The Effect ofJournal of oncology · 2021
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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

7 authors at 1 institution in 1 country.

Qun Dai *1Department of Pediatric, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510630 China.
Jingyi Deng *2Department of Emergency, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510630 China.
Jinrong Zhou2Department of Emergency, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510630 China.
Zhuhong Wang2Department of Emergency, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510630 China.
Xiao-Feng Yuan3Department of General Intensive Care Unit Medicine, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510630 China.
Shunwen Pan4Department of Laboratory Medicine, The Third Affiliated Hospital of Sun Yat-Sen University, No. 600, Tianhe Road, Guangzhou, 510630 China.ORCID 0000-0002-1266-4424
Hong-Bin Zhang4Department of Laboratory Medicine, The Third Affiliated Hospital of Sun Yat-Sen University, No. 600, Tianhe Road, Guangzhou, 510630 China.
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAccumulating evidence indicates that the long noncoding RNA taurine upregulated gene 1(TUG1) plays a critical role in cancer progression and metastasis. However, the overall biological role and clinical significance of TUG1 in hepatocellular carcinoma (HCC) remain largely unknown.

methodsThe expressions of TUG1, microRNA-216b-5p and distal-less homeobox 2 (DLX2) were detected by Quantitative real-time polymerase chain reaction (qRT-PCR). The target relationships were predicted by StarBase v.2.0 or TargetScan and confirmed by dual-luciferase reporter assay. The cell growth, apoptosis, migration and invasion were detected by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), Flow cytometry and Transwell assays, respectively. All protein expression levels were detected by western blot. Tumor xenografts were implemented to explore the role of TUG1 in vivo.

resultsWe found that there was a marked rise in TUG1 expression in HCC tissues and cells, and knockdown of TUG1 repressed the growth and metastasis and promoted apoptosis of HCC cells. In particular, TUG1 could act as a ceRNA, effectively becoming a sink for miR-216b-5p to fortify the expression of DLX2. Additionally, repression of TUG1 impared the progression of HCC cells by inhibiting DLX2 expression via sponging miR-216b-5p in vitro. More importantly, TUG1 knockdown inhibited HCC tumor growth in vivo through upregulating miR-216b-5p via inactivation of the DLX2.

conclusionTUG1 interacting with miR-216b-5p contributed to proliferation, metastasis, tumorigenesis and retarded apoptosis by activation of DLX2 in HCC.

Indexed as

DLX2HCCmiR-216b-5pTUG1

Identifiers

PMID31920462
PMCPMC6947942
OpenAlexW3000413306

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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.