Evidence map›Paper›PMID 33517826›Full record

ArticleBioengineered2021

Long non-coding RNA TTN antisense RNA 1 facilitates hepatocellular carcinoma progression via regulating miR-139-5p/SPOCK1 axis.

Xinghao Zhu, Shiqing Jiang, Zongyao Wu, Tonghua Liu, Wei Zhang, Lili Wu, Lijun Xu, Mingliang Shao

Open access · goldAbstract read
In one paragraph

Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
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  5. Making Sense of Antisense lncRNAs in Hepatocellular Carcinoma.International journal of molecular sciences · 2023
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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

8 authors at 4 institutions in 1 country.

Xinghao ZhuDepartment of Internal Medicine of Chinese Medicine, Henan University of Chinese Medicine , Zhengzhou, Henan, China.
Shiqing JiangThe First Affiliated Hospital of Henan University of Chinese Medicine , Zhengzhou, Henan, China.ORCID 0000-0001-9465-8070
Zongyao WuInstitute of Tibetan Medicine, Tibet University of Tibetan Medicine , Lhasa, Xizang, China.
Tonghua LiuBeijing University of Chinese Medicine , Beijing, China.
Wei ZhangInstitute of Liver Diseases, Shijiazhuang Fifth Hospital , Shijiazhuang, Hebei, China.
Lili WuBeijing University of Chinese Medicine , Beijing, China.
Lijun XuInstitute of Tibetan Medicine, Tibet University of Tibetan Medicine , Lhasa, Xizang, China.
Mingliang ShaoDepartment of Oncology, Shijiazhuang Fifth Hospital , Shijiazhuang, Hebei, China.
Beijing University of Chinese Medicine · CNFifth Hospital of Shijiazhuang · CNFirst Affiliated Hospital of Henan University · CNTibetan Traditional Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reportedly, long non-coding RNAs (lncRNAs) are implicated in hepatocellular carcinoma (HCC) progression, yet little is known concerning the biological functions of TTN antisense RNA 1 (TTN-AS1) in HCC. In this study, quantitative real-time polymerase chain reaction (qRT-PCR) was performed for detecting TTN-AS1, SPOCK1 mRNA, and miR-139-5p expressions in HCC cells and tissues. After TTN-AS1 was overexpressed or knocked down in HCC cells, CCK-8 and 5-Ethynyl-2'-deoxyuridine (EdU) assays were carried out for examining cell multiplication. Transwell assays were conducted for evaluating HCC cell migration and invasion. Dual-luciferase reporter assay was employed for verifying the binding relationships between miR-139-5p and TTN-AS1, and between SPOCK1 3'UTR and miR-139-5p. Western blot was employed to measure SPOCK1, E-cadherin, N-cadherin, and Vimentin protein expressions. We demonstrated that, TTN-AS1 and SPOCK1 expression levels were remarkably enhanced in HCC cells and tissues, whereas miR-139-5p expression was observably reduced. Functional experiments suggested that TTN-AS1 knockdown markedly repressed HCC cell multiplication, migration, epithelial-mesenchymal transition (EMT), and invasion. In addition, TTN-AS1 interacted with miR-139-5p and decreased its expression. Moreover, SPOCK1 was a miR-139-5p target, and miR-139-5p inhibitors were able to reverse TTN-AS1 knockdown-induced inhibitory effect on SPOCK1 expression. SPOCK1 overexpression plasmid could counteract TTN-AS1 knockdown-induced inhibiting impact on HCC cell multiplication, migration, invasion, and EMT. In conclusion, TTN-AS1 expression level is remarkably enhanced in HCC, and TTN-AS1 can promote the multiplication, migration, invasion, and EMT of HCC cells via regulating miR-139-5p/SPOCK1 axis.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsMicroRNAsRNA, AntisenseRNA, Long NoncodingCell Line, TumorDisease ProgressionEpithelial-Mesenchymal TransitionFemaleGene Knockdown TechniquesHumansLiverMaleMiddle AgedProteoglycansMicroRNAsMIRN139 microRNA, humanProteoglycansRNA, AntisenseRNA, Long NoncodingSPOCK1 protein, humanEMThepatocellular carcinoma (HCC)MiR-139-5pSPOCK1TTN-AS1

Identifiers

PMID33517826
PMCPMC8291788
OpenAlexW3128124292

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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.