Evidence map›Paper›PMID 30489194›Full record

ArticleCancer biology & therapy2019

Upregulation of long non-coding RNA NNT-AS1 promotes osteosarcoma progression by inhibiting the tumor suppressive miR-320a.

Changhui Li, Shouyun Zhang, Tongguo Qiu, Yuanji Wang, David M Ricketts, Chao Qi

RetractedOpen access · bronzeAbstract readRetracted Publication
In one paragraph

Article in Cancer biology & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
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

21 citing papers in PubMed, 38 citations in OpenAlex.

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  17. Overexpression of NNT-AS1 Activates TGF-BioMed research international · 2020
    Article
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  19. Long noncoding RNAAging · 2019
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Changhui Lia Department of Orthopedics , People's Hospital of Rizhao , Shandong , China.
Shouyun Zhanga Department of Orthopedics , People's Hospital of Rizhao , Shandong , China.
Tongguo Qiub Department of medicine , Kuishan branch of People's Hospital of Rizhao , Shandong , China.
Yuanji Wanga Department of Orthopedics , People's Hospital of Rizhao , Shandong , China.
David M Rickettsc Department of Orthopedics , Brighton and Sussex University Hospitals , UK.
Chao Qid Department of Orthopedics , Affiliated Hospital of Qingdao University , Shandong , China.
People’s Hospital of Rizhao · CNAffiliated Hospital of Qingdao University · CNUniversity Hospitals Sussex NHS Foundation Trust · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate the role and mechanism of action of nicotinamide nucleotide transhydrogenase antisense RNA 1 (NNT-AS1) in osteosarcoma (OS).

methodsBioinformatic analysis suggested miR-320a as potential target of NNT-AS1. Influence of NNT-AS1 overexpression or knockdown on OS cell proliferation, colony-formation, apoptosis, migration and invasion capacity was first investigated. Expression levels of NNT-AS1, miR-320a, beta-catenin, RUNX2, IGF-1R, c-Myc, Cyclin D1 and MMP13 were also evaluated by RT-qPCR and western blotting accordingly. Xenograft models using U2OS and OS-732 cells with different NNT-AS1 gene modifications were constructed for tumor formation assay as well as evaluation of miR-320a, beta-catenin and RUNX2 expression in primary lesion. NNT-AS1-overexpressing U2OS cells and NNT-AS1-knockdown OS-732 cells were subject to miR-320a mimic and inhibitor transfection, respectively, to investigate the miR-320a dependency of the osteosarcoma-promoting role of NNT-AS1.

resultsNNT-AS1 overexpression significantly increased proliferation, survival and mobility of U2OS cells in vitro as well as its tumor formation ability in vivo, while NNT-AS1 knockdown showed opposite effect on OS-732 cells. In both in vitro and in vivo model, NNT-AS1 expression level significantly correlated with that of beta-catenin, RUNX2, IGF-1R, c-Myc, Cyclin D1 and MMP13 as well as Akt phosphorylation level, and inversely correlated with miR-320a expression. Transfection of miR-320a mimic significantly inhibiter the promoting effect of NNT-AS1 on cell proliferation, survival and mobility of U2OS cells, while miR-320 inhibitor partially rescued that of OS-732 cells.

conclusionNNT-As1 functions as a cancer-promoting lncRNA by downregulating miR-320a, thus increasing the protein expression level of beta-catenin, RUNX2 and IGF-1R as well as activation of Akt in osteosarcoma.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisbeta CateninBiomarkers, TumorBone NeoplasmsCell ProliferationCore Binding Factor Alpha 1 SubunitHumansMiceMice, NudeMicroRNAsMitochondrial ProteinsNADP Transhydrogenase, AB-SpecificOsteosarcomaRNA, Antisensebeta CateninBiomarkers, TumorCore Binding Factor Alpha 1 SubunitCTNNB1 protein, humanMicroRNAsMIRN320 microRNA, humanMitochondrial ProteinsNADP Transhydrogenase, AB-SpecificNNT protein, humanRNA, AntisenseRNA, Long NoncodingRUNX2 protein, humanlong noncoding RNAmiR-320aNNT-AS1osteosarcoma

Identifiers

PMID30489194
PMCPMC6422455
OpenAlexW2903416633

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.