Evidence map›Paper›PMID 38914506›Full record

ArticleInternational dental journal2024

LncRNA AFAP1-AS1 Promotes Oral Squamous Cell Carcinoma Development by Ubiquitin-Mediated Proteolysis.

Bao-Jun Li, Feng-Hai Ren, Cui Zhang, Xing-Wei Zhang, Xiao-Hui Jiao

Abstract read
In one paragraph

Article in International dental journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

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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

4 citing papers in PubMed.

  1. AFAP1-AS1 regulates oral squamous cell carcinoma development through the miR-93-3p/CCND1 signaling pathway.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Article
  2. Article
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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

5 authors.

Bao-Jun LiDepartment of Head and Neck Surgery, Harbin Medical University Cancer Hospital, Harbin, China.
Feng-Hai RenDepartment of Thoracic Surgery, Harbin Medical University Cancer Hospital, Harbin, China.
Cui ZhangDepartment of Medical Ultrasound, Harbin Medical University Cancer Hospital, Harbin, China.
Xing-Wei ZhangDepartment of Oral and Maxillofacial Surgery, The First Affiliate Hospital of Harbin Medical University, Harbin, China.
Xiao-Hui JiaoDepartment of Oral and Maxillofacial Surgery, The First Affiliate Hospital of Harbin Medical University, Harbin, China. Electronic address: jiaoxiaohui_doctor@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeLong noncoding RNA (lncRNA) dysregulation has been reported to play a pivotal role in the development of cancers. In this study, we aimed to screen the key lncRNA in oral squamous cell carcinoma (OSCC) via bioinformatics analysis and further validate the function of lncRNA in vitro and in vivo.

methodsBioinformatics analysis was conducted to identify differentially expressed lncRNAs between control and OSCC samples. Quantitative real-time-polymerase chain reaction was employed to detect the expression of differentially expressed lncRNAs in human tongue squamous cell carcinoma and human oral keratinocytes cell lines. The biological function of lncRNA and its mechanism were examined via the experimental assessment of the cell lines with the lncRNA overexpressed and silenced. Additionally, to further explore the function of lncRNA in the progression of OSCC, xenograft tumour mouse models were established using 25 mice (5 groups, each with 5 mice). Tumour formation was observed at 2 weeks after the cell injection, and the tumours were resected at 5 weeks post-implantation.

resultsTwo lncRNAs, LINC00958 and AFAP1-AS1, were found to be correlated with the prognosis of OSCC. The results of the quantitative real-time-polymerase chain reaction indicated that the 2 lncRNAs were highly expressed in OSCC. In combination with the previous literature, we found AFAP1-AS1 to be a potentially important biomarker for OSCC. Thus, we further investigated its biological function and found that AFAP1-AS1 silencing inhibited cell proliferation, migration, and invasion whereas AFAP1-AS1 overexpression reversed the effect of AFAP1-AS1 silencing (P < .05). Mechanism analysis revealed that AFAP1-AS1 regulated the development of OSCC through the ubiquitin-mediated proteolysis pathway.

conclusionsAFAP1-AS1 is an oncogene that aggravates the development of OSCC via the ubiquitin-mediated proteolysis pathway. It also provides a novel potential therapy for OSCC.

Indexed as

Carcinoma, Squamous CellMouth NeoplasmsRNA, Long NoncodingUbiquitinAnimalsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansMiceMice, NudePrognosisProteolysisReal-Time Polymerase Chain ReactionTongue NeoplasmsAFAP1-AS1 long noncoding RNA, humanRNA, Long NoncodingUbiquitinLong noncoding RNAMalignant tumour characteristicsOral squamous cell carcinomaUbiquitin conjugating enzyme E2 D2

Identifiers

PMID38914506
PMCPMC11551608

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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.