Evidence map›Paper›PMID 32086979›Full record

ArticleCancer science2020

MicroRNA-361-3p is a potent therapeutic target for oral squamous cell carcinoma.

Himiko Ogawa, Koh-Ichi Nakashiro, Norihiko Tokuzen, Nobuyuki Kuribayashi, Hiroyuki Goda, Daisuke Uchida

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed, 29 citations in OpenAlex.

  1. MicroRNA in cancer therapy: breakthroughs and challenges in early clinical applications.Journal of experimental & clinical cancer research : CR · 2025
    Review
  2. Article
  3. Targeted gene therapy for cancer: the impact of microRNA multipotentiality.Medical oncology (Northwood, London, England) · 2024
    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

6 authors at 1 institution in 1 country.

Himiko OgawaDepartment of Oral and Maxillofacial Surgery, Ehime University Graduate School of Medicine, Toon, Japan.
Koh-Ichi NakashiroDepartment of Oral and Maxillofacial Surgery, Ehime University Graduate School of Medicine, Toon, Japan.ORCID https://orcid.org/0000-0002-9975-902X
Norihiko TokuzenDepartment of Oral and Maxillofacial Surgery, Ehime University Graduate School of Medicine, Toon, Japan.
Nobuyuki KuribayashiDepartment of Oral and Maxillofacial Surgery, Ehime University Graduate School of Medicine, Toon, Japan.
Hiroyuki GodaDepartment of Oral and Maxillofacial Surgery, Ehime University Graduate School of Medicine, Toon, Japan.
Daisuke UchidaDepartment of Oral and Maxillofacial Surgery, Ehime University Graduate School of Medicine, Toon, Japan.
Ehime University · JP

Funding

JSPS KAKENHI 24390457
6 · The paper itself

Abstract

MicroRNAs (miRNAs) can act not only as tumor suppressor genes but also as oncogenes. Oncogenic miRNAs (oncomiRs) could therefore provide opportunities for the treatment of human malignancies. Here, we aimed to identify oncomiRs present in oral squamous cell carcinoma (OSCC) and addressed whether targeting these miRNAs might be useful in treatment for cancer. Functional screening for oncomiRs in a human OSCC cell line (GFP-SAS) was carried out using the miRCURY LNA microRNA Knockdown Library - Human version 12.0. We identified a locked nucleic acid (LNA)/DNA antisense oligonucleotide against miR-361-3p (LNA-miR-361-3p) which showed the largest degree of growth inhibition of GFP-SAS cells. Transfection with a synthetic mimic of mature miR-361-3p resulted in an approximately 20% increase in the growth of GFP-SAS cells. We identified odd-skipped related 2 (OSR2) as a miR-361-3p target gene. Transfection of GFP-SAS cells with LNA-miR-361-3p caused a significant increase in the expression levels of OSR2. Cotransfection of a OSR2 3'-UTR luciferase reporter plasmid and LNA-miR-361-3p into GFP-SAS cells produced higher levels of luciferase activity than in cells cotransfected with the LNA-nontarget. We assessed the effect of LNA-miR-361-3p on the in vivo growth of GFP-SAS cells. We found that LNA-miR-361-3p significantly reduced the size of s.c. xenografted GFP-SAS tumors, compared to the control group treated with LNA-NT. Finally, we observed that miR-361-3p is overexpressed in OSCC tissues. These results suggest that miR-361-3p supports the growth of human OSCC cells both in vitro and in vivo and that targeting miR-361-3p could be a useful therapeutic approach for patients with OSCC.

Indexed as

AnimalsCarcinogenesisCarcinoma, Squamous CellCell Line, TumorCell ProliferationFemaleGene ExpressionGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeMicroRNAsMouth NeoplasmsOligonucleotidesTranscription Factorslocked nucleic acidMicroRNAsMIRN361 microRNA, humanOligonucleotidesOSR2 protein, humanTranscription FactorsLNA/DNA antisense oligonucleotidemicroRNAmiR-361-3poncomiRoral squamous cell carcinoma

Identifiers

PMID32086979
PMCPMC7226181
OpenAlexW3007621409

What OpenQuestion holds

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LicenceCC BY-NC
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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.