Evidence map›Paper›PMID 26243299›Full record

ArticleJournal of experimental & clinical cancer research : CR2015

microRNA-93 promotes cell proliferation via targeting of PTEN in Osteosarcoma cells.

Masanori Kawano, Kazuhiro Tanaka, Ichiro Itonaga, Shinichi Ikeda, Tatsuya Iwasaki, Hiroshi Tsumura

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 6% 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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.

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  9. MiRNA-93: a novel signature in human disorders and drug resistance.Cell communication and signaling : CCS · 2023
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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.

Masanori KawanoDepartment of Orthopaedic Surgery, Faculty of Medicine, Oita University, Oita, 879-5593, Japan. kawano@oita-u.ac.jp.
Kazuhiro TanakaDepartment of Orthopaedic Surgery, Faculty of Medicine, Oita University, Oita, 879-5593, Japan. ktanaka@oita-u.ac.jp.
Ichiro ItonagaDepartment of Orthopaedic Surgery, Faculty of Medicine, Oita University, Oita, 879-5593, Japan. itonaga@oita-u.ac.jp.
Shinichi IkedaDepartment of Orthopaedic Surgery, Faculty of Medicine, Oita University, Oita, 879-5593, Japan. ike@oita-u.ac.jp.
Tatsuya IwasakiDepartment of Orthopaedic Surgery, Faculty of Medicine, Oita University, Oita, 879-5593, Japan. tatsuya@oita-u.ac.jp.
Hiroshi TsumuraDepartment of Orthopaedic Surgery, Faculty of Medicine, Oita University, Oita, 879-5593, Japan. htsumura@oita-u.ac.jp.
Oita University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAberrant microRNA (miRNA) expression plays an essential role in osteosarcoma (OS) pathogenesis. Recent studies have shown that dysregulation of miRNA expression is associated with increased tumorigenesis and poor prognosis in several types of cancers, including OS. The aim of this study was to investigate the relevant microRNAs involved in the development of OS.

methodsTo explore possible oncogenic factors in OS, we used a microarray-based approach to profile changes in the expression of miRNAs and their target mRNAs in five OS cell lines and human mesenchymal stem cells (hMSCs). An miRNA, miR-93, was significantly up-regulated, whereas phosphatase and tensin homologue (PTEN) expression was significantly down-regulated in all tested OS cells, when compared with hMSCs.

resultsWhen anti-miR-93 was transfected into OS cell lines, PTEN expression was greatly increased, suggesting that PTEN might be a target of miR-93 in ES cells. The expression of phosphorylated Akt protein, which is known to be inversely correlated with that of PTEN, was significantly down-regulated in anti-miR-93-transfected cells. Furthermore, transfection of anti-miR-93 inhibited the proliferation and cell cycle progression of ES cells. In addition, the down-regulation of miR-93 in these cells significantly suppressed tumor growth in vivo.

conclusionEctopic expression of miR-93 decreased PTEN protein levels. Furthermore, miR-93 increased proliferation and decreased apoptosis in OS cells, whereas its silencing in these cells inhibited such carcinogenic processes. Taking these observations together, miR-93 can be seen to play a critical role in carcinogenesis through suppression of PTEN, and may serve as a therapeutic target for the treatment of OS.

Indexed as

AnimalsApoptosisCell Line, TumorCell ProliferationHumansMiceMice, Inbred BALB CMicroRNAsOsteosarcomaPTEN PhosphohydrolaseTransfectionMicroRNAsPTEN PhosphohydrolasePTEN protein, human

Identifiers

PMID26243299
PMCPMC4524362
OpenAlexW1857894653

What OpenQuestion holds

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LicenceCC BY
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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.