Evidence map›Paper›PMID 32948745›Full record

ArticleCell death & disease2020

CCL18-induced LINC00319 promotes proliferation and metastasis in oral squamous cell carcinoma via the miR-199a-5p/FZD4 axis.

Xiao Jiang, Jingpeng Liu, Simin Li, Bo Jia, Zhijie Huang, Jun Shen, Haiyun Luo, Jianjiang Zhao

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
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  3. Deciphering the multifaceted role ofFrontiers in immunology · 2025
    Article
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  5. Circ_0070934 promotes MGAT3 expression and inhibits epithelial-mesenchymal transition in bronchial epithelial cells by sponging miR-199a-5p.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2024
    Article
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  14. Noncoding RNAs as sensors of tumor microenvironmental stress.Journal of experimental & clinical cancer research : CR · 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

8 authors at 2 institutions in 1 country.

Xiao JiangStomatological Hospital, Southern Medical University, Guangzhou, Guangdong, China.ORCID http://orcid.org/0000-0001-6893-9370
Jingpeng LiuStomatological Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Simin LiStomatological Hospital, Southern Medical University, Guangzhou, Guangdong, China.ORCID http://orcid.org/0000-0003-4011-0282
Bo JiaStomatological Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Zhijie HuangStomatological Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Jun ShenStomatological Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Haiyun LuoStomatological Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Jianjiang ZhaoStomatological Hospital, Southern Medical University, Guangzhou, Guangdong, China. zjj2521@sina.com.ORCID http://orcid.org/0000-0003-2363-2935
Southern Medical University · CNGuangdong Province Stomatological Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long non-coding RNAs (lncRNAs), which may be modulated by chemokines, are key regulators in many cancers including oral squamous cell carcinoma (OSCC). An understanding of lncRNAs involved in chemokine (CC motif) ligand 18 (CCL18)-induced OSCC promotion remains elusive. The present study using lncRNA sequencing found LINC00319 to be significantly upregulated in OSCC cells subjected to rCCL18 stimulation. Furthermore, LINC00319 knockdown was found to attenuate the carcinogenic function of CCL18 in OSCC, reducing OSCC proliferation, metastasis, epithelial-mesenchymal transition (EMT), and angiogenesis. LINC00319 was demonstrated to act as a ceRNA in OSCC, which directly responded to miR-199a-5p and rescued the repression of FZD4 by miR-199a-5p. Functionally, in vitro and in vivo experiments showed that LINC00319 promoted OSCC growth and metastasis via downregulating miR-199a-5p and upregulating FZD4. In vitro rescue assays demonstrated that miR-199a-5p inhibitor or FZD4 overexpression reversed the effects of LINC00319 silencing in OSCC. Importantly, the expression of miR-199a-5p and FZD4 were found to be mediated by CCL18, and miR-199a-5p mimics inhibited the CCL18-promoting effects in oral cancer cells. Taken together, these results evidenced a mechanism of CCL18 action in OSCC mediated through the LINC00319/miR-199a-5p/FZD4 signaling pathway, which may comprise a potential target for OSCC therapeutic development.

Indexed as

CarcinogenesisCarcinoma, Squamous CellCell MovementCell ProliferationChemokines, CCFrizzled ReceptorsGene Expression Regulation, NeoplasticHumansMicroRNAsNeoplasm MetastasisRNA, Long NoncodingSquamous Cell Carcinoma of Head and NeckCCL18 protein, humanChemokines, CCFrizzled ReceptorsFZD4 protein, humanLINC00339 long noncoding RNA, humanMicroRNAsmirn199 microRNA, humanRNA, Long Noncoding

Identifiers

PMID32948745
PMCPMC7501282
OpenAlexW3087151726

What OpenQuestion holds

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LicenceCC BY
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.