Evidence map›Paper›PMID 32042127›Full record

ArticleGene therapy2019

LncRNA OIP5-AS1 interacts with miR-363-3p to contribute to hepatocellular carcinoma progression through up-regulation of SOX4.

Jianchu Wang, Qianli Tang, Libai Lu, Zongjiang Luo, Wenchuan Li, Yuan Lu, Jian Pu

Abstract read
PubMed Publisher
In one paragraph

Article in Gene therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

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  11. The role of lncRNA OIP5-AS1 in cancer development and progression.Apoptosis : an international journal on programmed cell death · 2022
    Review
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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.

Jianchu WangDepartment of Hepatobiliary Surgery, Affiliated Hospital of Youjiang Medical University for Nationalities, No. 18 Zhongshan Road, Baise, 533000, Guangxi Zhuang Autonomous Region, China.
Qianli TangDepartment of Hepatobiliary Surgery, Affiliated Hospital of Youjiang Medical University for Nationalities, No. 18 Zhongshan Road, Baise, 533000, Guangxi Zhuang Autonomous Region, China.
Libai LuDepartment of Hepatobiliary Surgery, Affiliated Hospital of Youjiang Medical University for Nationalities, No. 18 Zhongshan Road, Baise, 533000, Guangxi Zhuang Autonomous Region, China.
Zongjiang LuoDepartment of Hepatobiliary Surgery, Affiliated Hospital of Youjiang Medical University for Nationalities, No. 18 Zhongshan Road, Baise, 533000, Guangxi Zhuang Autonomous Region, China.
Wenchuan LiDepartment of Hepatobiliary Surgery, Affiliated Hospital of Youjiang Medical University for Nationalities, No. 18 Zhongshan Road, Baise, 533000, Guangxi Zhuang Autonomous Region, China.
Yuan LuDepartment of Hepatobiliary Surgery, Affiliated Hospital of Youjiang Medical University for Nationalities, No. 18 Zhongshan Road, Baise, 533000, Guangxi Zhuang Autonomous Region, China.
Jian PuDepartment of Hepatobiliary Surgery, Affiliated Hospital of Youjiang Medical University for Nationalities, No. 18 Zhongshan Road, Baise, 533000, Guangxi Zhuang Autonomous Region, China. pujianym@163.com.
Affiliated Hospital of Youjiang Medical University for Nationalities · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long noncoding RNA OIP5-AS1 has been observed to be increased in several cancers, however, its role and biological mechanism was poorly understood in HCC. Currently, we found OIP5-AS1 expression was upregulated in HCC cells compared with normal human liver cells. Knockdown of OIP5-AS1 suppressed HCC cell proliferation, induced cells cycle arrest and cells apoptosis. In addition, HCC cell migration and invasion capacity in vitro were also inhibited by OIP5-AS1 inhibition. Bioinformatics analysis revealed OIP5-AS1 could interact with miR-363-3p, thereby repressing HCC development. We also observed miR-363-3p was significantly decreased in HCC cells and overexpression of miR-363-3p repressed HCC progression. The correlation between OIP5-AS1 and miR-363-3p was confirmed by performing RIP assay and RNA pull-down assay. Subsequently, SOX4 was predicted as a target of miR-363-3p and miR-363-3p modulated SOX4 levels negatively in vitro. Apart from these, in vivo experiments established that OIP5-AS1 can suppress HCC development through regulating miR-363-3p and SOX4. Collectively, these demonstrated that OIP5-AS1 was involved in HCC progression via targeting miR-363-3p and SOX4. OIP5-AS1 can act as a novel candidate for HCC diagnosis, prognosis, and therapy.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsMicroRNAsRNA, Long NoncodingCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansSOXC Transcription FactorsUp-Regulationlong noncoding RNA OIP5, humanMicroRNAsMIRN363 microRNA, humanRNA, Long NoncodingSOX4 protein, humanSOXC Transcription Factors

Identifiers

PMID32042127
OpenAlexW3004970357

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.