Evidence map›Paper›PMID 34713296›Full record

ArticleInternational journal of oncology2021

Regulatory roles of miRNAs 16, 133a, and 223 on osteoclastic bone destruction caused by breast cancer metastasis.

Kazumichi Kitayama, Teruya Kawamoto, Yohei Kawakami, Hitomi Hara, Toshiyuki Takemori, Shuichi Fujiwara, Shunsuke Yahiro, Tomohiro Miyamoto, Yutaka Mifune, Yuichi Hoshino and 6 more

Open access · hybridAbstract read
In one paragraph

Article in International journal of oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 42% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
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  7. Muscle and Bone Defects in Metastatic Disease.Current osteoporosis reports · 2022
    Review
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

16 authors at 1 institution in 1 country.

Kazumichi KitayamaDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Kobe, Hyogo 650‑0017, Japan.
Teruya KawamotoDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Kobe, Hyogo 650‑0017, Japan.
Yohei KawakamiDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Kobe, Hyogo 650‑0017, Japan.
Hitomi HaraDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Kobe, Hyogo 650‑0017, Japan.
Toshiyuki TakemoriDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Kobe, Hyogo 650‑0017, Japan.
Shuichi FujiwaraDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Kobe, Hyogo 650‑0017, Japan.
Shunsuke YahiroDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Kobe, Hyogo 650‑0017, Japan.
Tomohiro MiyamotoDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Kobe, Hyogo 650‑0017, Japan.
Yutaka MifuneDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Kobe, Hyogo 650‑0017, Japan.
Yuichi HoshinoDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Kobe, Hyogo 650‑0017, Japan.
Kenichiro KakutaniDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Kobe, Hyogo 650‑0017, Japan.
Tomoyuki MatsumotoDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Kobe, Hyogo 650‑0017, Japan.
Takehiko MatsushitaDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Kobe, Hyogo 650‑0017, Japan.
Takahiro NiikuraDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Kobe, Hyogo 650‑0017, Japan.
Ryosuke KurodaDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Kobe, Hyogo 650‑0017, Japan.
Toshihiro AkisueDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Kobe, Hyogo 650‑0017, Japan.
Kobe University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteolytic bone metastasis leads to skeletal‑related events, resulting in a decline in the patient activities and survival; therefore, it is important to understand the mechanism underlying bone metastasis. Recent studies have suggested that microRNAs (miRNAs or miRs) are involved in osteoclast differentiation and/or osteolytic bone metastasis; however, the roles of miRNAs have not been elucidated. In the present study, the roles of miRNAs in bone destruction caused by breast cancer metastasis were investigated

Indexed as

Gene Expression Regulation, NeoplasticAnimalsBiomarkers, TumorBone NeoplasmsBreast NeoplasmsCell Line, TumorFemaleHumansMiceMice, NudeMicroRNAsOsteoclastsOsteolysisRAW 264.7 CellsTumor MicroenvironmentXenograft Model Antitumor AssaysBiomarkers, TumorMicroRNAsMIR223, humanMIRN133 microRNA, humanMIRN16 microRNA, humanbone metastasisbreast cancermicroRNAmicroRNA‑133amicroRNA‑16microRNA‑223osteoclast

Identifiers

PMID34713296
PMCPMC8562387
OpenAlexW3209476276

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.