Evidence map›Paper›PMID 35293593›Full record

ArticleOncology reports2022

miRNA‑218 targets multiple oncogenes and is a therapeutic target for osteosarcoma.

Kentaro Sato, Eiji Osaka, Kyoko Fujiwara, Ryota Fujii, Tadateru Takayama, Yasuaki Tokuhashi, Kazuyoshi Nakanishi

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Kentaro SatoDepartment of Orthopedic Surgery, Nihon University Hospital, Chiyoda‑ku, Tokyo 101‑8309, Japan.
Eiji OsakaDepartment of Orthopedic Surgery, Nihon University School of Medicine, Itabashi‑ku, Tokyo 173‑8610, Japan.
Kyoko FujiwaraDepartment of Internal Medicine, Nihon University School of Medicine, Itabashi‑ku, Tokyo 173‑8610, Japan.
Ryota FujiiDepartment of Orthopedic Surgery, Nihon University School of Medicine, Itabashi‑ku, Tokyo 173‑8610, Japan.
Tadateru TakayamaDepartment of Internal Medicine, Nihon University School of Medicine, Itabashi‑ku, Tokyo 173‑8610, Japan.
Yasuaki TokuhashiDepartment of Orthopedic Surgery, Tachikawa Kinen Hospital, Kasama City, Ibaraki 309‑1736, Japan.
Kazuyoshi NakanishiDepartment of Orthopedic Surgery, Nihon University School of Medicine, Itabashi‑ku, Tokyo 173‑8610, Japan.
Nihon University · JPTachikawa Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Survivin is overexpressed in various cancers and is correlated with treatment resistance and prognosis. MicroRNAs (miRNAs) directly regulate several target genes and are potential therapeutic agents for various cancers. The present study evaluated multiple gene targets of miR‑218, including survivin, in osteosarcoma and compared the anti‑tumor effects of miR‑218 with those of YM155, an anti‑survivin agent. It assessed the expression levels of miR‑218 and survivin in osteosarcoma and osteoblast cell lines, as well as the proliferative, migratory and invasive capacities of cells following treatment with miR‑218 or YM155. The form of cell death was assessed using fluorescence‑activated cell sorting analysis to examine the expression of invasion ability‑related genes. Osteosarcoma cell lines were subcutaneously injected into immunodeficient mice; the mice were then treated with miR‑218 or YM155 to assess the anti‑tumor effects of these agents. The results showed that miR‑218 was downregulated, whereas survivin was overexpressed in the osteosarcoma cell line compared with normal osteoblast cells. The expression of survivin was suppressed upon overexpression of miR‑218 (miR‑218 group) or administration of YM155 (YM155 group), leading to apoptosis and inhibition of osteosarcoma cell proliferation. Invasion and migration abilities were inhibited in the miR‑218 group, but not in the YM155 group. In the animal model, both the miR‑218 and YM155 groups showed a reduced tumor volume and decreased survivin expression. In osteosarcoma, miR‑218 showed a wider range of therapeutic efficacy compared with YM155, suggesting that miR‑218 should be evaluated as a treatment target.

Indexed as

Bone NeoplasmsMicroRNAsOncogenesOsteosarcomaAnimalsCell Line, TumorMiceMicroRNAsMIRN218 microRNA, mousemiR‑218osteosarcomasurvivintargeted therapyYM155

Identifiers

PMID35293593
PMCPMC8968766
OpenAlexW4220839817

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.