Evidence map›Paper›PMID 33442262›Full record

ArticleOncoTargets and therapy2021

Long Noncoding RNA CCDC144NL-AS1 Promotes the Oncogenicity of Osteosarcoma by Acting as a Molecular Sponge for microRNA-490-3p and Thereby Increasing HMGA2 Expression.

Juliang He, Jian Guan, Shian Liao, Zhenjie Wu, Bin Liu, Hao Mo, Zhenchao Yuan

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in OncoTargets and therapy, 2021. 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 It has been retracted, and should not be counted.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 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.5field-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

10 citing papers in PubMed, 18 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Juliang He *Department of Bone and Soft Tissue Surgery, Guangxi Medical University Cancer Hospital, Nanning, Guangxi 530021, People's Republic of China.
Jian Guan *Department of Bone and Soft Tissue Surgery, Guangxi Medical University Cancer Hospital, Nanning, Guangxi 530021, People's Republic of China.ORCID 0000-0003-1739-4328
Shian LiaoDepartment of Bone and Soft Tissue Surgery, Guangxi Medical University Cancer Hospital, Nanning, Guangxi 530021, People's Republic of China.
Zhenjie WuDepartment of Bone and Soft Tissue Surgery, Guangxi Medical University Cancer Hospital, Nanning, Guangxi 530021, People's Republic of China.
Bin LiuDepartment of Bone and Soft Tissue Surgery, Guangxi Medical University Cancer Hospital, Nanning, Guangxi 530021, People's Republic of China.
Hao MoDepartment of Bone and Soft Tissue Surgery, Guangxi Medical University Cancer Hospital, Nanning, Guangxi 530021, People's Republic of China.
Zhenchao YuanDepartment of Bone and Soft Tissue Surgery, Guangxi Medical University Cancer Hospital, Nanning, Guangxi 530021, People's Republic of China.
Guangxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe long noncoding RNA CCDC144NL antisense RNA 1 (CCDC144NL-AS1) exhibits important functions in gastric cancer. In this study, we aimed to investigate the roles of CCDC144NL-AS1 in modulating the phenotype of osteosarcoma (OS) cells in vitro and in vivo and elucidate its underlying mechanisms.

methodsReverse transcription quantitative polymerase chain reaction (PCR) was performed to determine the expression level of CCDC144NL-AS1 in OS tissues and cell lines. The proliferation, apoptosis, migration, and invasion in vitro as well as tumor growth in vivo were determined in OS cells using the Cell Counting Kit 8 assay, flow cytometric analysis, transwell migration and invasion assays, and xenograft experiments, respectively. Bioinformatics analysis was performed to identify the potential microRNA targets of CCDC144NL-AS1, which were subsequently confirmed using the luciferase reporter assay, RNA immunoprecipitation assay, reverse transcription quantitative PCR, Western blotting, and rescue experiments.

resultsCCDC144NL-AS1 expression was upregulated in OS tissues and cell lines. Patients with OS who exhibited high CCDC144NL-AS1 expression had shorter overall survival than those who exhibited low CCDC144NL-AS1 expression. Functionally, interference in CCDC144NL-AS1 expression led to a notable decrease in the proliferation, migration, and invasion of OS cells and an increase in cell apoptosis in vitro. Furthermore, CCDC144NL-AS1 knockdown impaired OS tumor growth in vivo. Mechanistically, CCDC144NL-AS1 directly bound to miR-490-3p in OS cells, where it functioned as a molecular sponge and subsequently increased the expression of high-mobility group AT-hook 2 (HMGA2). Rescue experiments further demonstrated that miR-490-3p suppression or HMGA2 restoration abated CCDC144NL-AS1 deficiency-induced cancer-inhibitory actions in OS cells.

conclusionCCDC144NL-AS1 exhibits pro-oncogenic roles in OS by functioning as a sponge for miR-490-3p and increasing HMGA2 expression. Our findings suggest that greater understanding of the CCDC144NL-AS1/miR-490-3p/HMGA2 pathway can provide useful information for OS diagnosis, prognosis, and therapy.

Indexed as

competitive endogenous RNAhigh-mobility group AT-hook 2long noncoding RNAmicroRNA

Identifiers

PMID33442262
PMCPMC7797336
OpenAlexW3120382110

What OpenQuestion holds

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LicenceCC BY-NC
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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.