Evidence map›Paper›PMID 32299427›Full record

ArticleReproductive biology and endocrinology : RB&E2020

hsa-miR-100-5p, an overexpressed miRNA in human ovarian endometriotic stromal cells, promotes invasion through attenuation of SMARCD1 expression.

Kanetoshi Takebayashi, Kaei Nasu, Mamiko Okamoto, Yoko Aoyagi, Tomoko Hirakawa, Hisashi Narahara

Open access · goldAbstract read
In one paragraph

Article in Reproductive biology and endocrinology : RB&E, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 30 citations in OpenAlex.

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  11. The roles of chromatin regulatory factors in endometriosis.Journal of assisted reproduction and genetics · 2024
    Review
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  14. miR-100-5p Regulates Skeletal Muscle Myogenesis through theInternational journal of molecular sciences · 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.

Kanetoshi TakebayashiDepartment of Obstetrics and Gynecology, Faculty of Medicine, Oita University, Idaigaoka 1-1, Hasama-machi, Yufu-shi, Oita, 879-5593, Japan.
Kaei NasuDepartment of Obstetrics and Gynecology, Faculty of Medicine, Oita University, Idaigaoka 1-1, Hasama-machi, Yufu-shi, Oita, 879-5593, Japan. nasu@oita-u.ac.jp.
Mamiko OkamotoDepartment of Obstetrics and Gynecology, Faculty of Medicine, Oita University, Idaigaoka 1-1, Hasama-machi, Yufu-shi, Oita, 879-5593, Japan.
Yoko AoyagiDepartment of Obstetrics and Gynecology, Faculty of Medicine, Oita University, Idaigaoka 1-1, Hasama-machi, Yufu-shi, Oita, 879-5593, Japan.
Tomoko HirakawaDepartment of Obstetrics and Gynecology, Faculty of Medicine, Oita University, Idaigaoka 1-1, Hasama-machi, Yufu-shi, Oita, 879-5593, Japan.
Hisashi NaraharaDepartment of Obstetrics and Gynecology, Faculty of Medicine, Oita University, Idaigaoka 1-1, Hasama-machi, Yufu-shi, Oita, 879-5593, Japan.
Oita University · JP

Funding

Japan Society for the Promotion of Science 15K10679Japan Society for the Promotion of Science 17K16857Japan Society for the Promotion of Science 18K16774Japan Society for the Promotion of Science no. 16K11093
6 · The paper itself

Abstract

backgroundA number of microRNAs are aberrantly expressed in endometriosis and are involved in its pathogenesis. Our previous study demonstrated that has-miR-100-5p expression is enhanced in human endometriotic cyst stromal cells (ECSCs). The present study aimed to elucidate the roles of has-miR-100-5p in the pathogenesis of endometriosis.

methodsNormal endometrial stromal cells (NESCs) were isolated from normal eutopic endometrium without endometriosis. Using hsa-miR-100-5p-transfected NESCs, we evaluated the effect of hsa-miR-100-5p on the invasiveness of these cells by Transwell invasion assay and in-vitro wound repair assay. We also investigated the downstream signal pathways of hsa-miR-100-5p by microarray analysis and Ingenuity pathways analysis.

resultshsa-miR-100-5p transfection enhanced the invasion and motility of NESCs. After hsa-miR-100-5p transfection, mRNA expression of SWItch/sucrose non-fermentable-related matrix-associated actin-dependent regulator of chromatin subfamily D member 1 (SMARCD1) was significantly attenuated. Whereas, the expression of matrix metallopeptidase 1 (MMP1) mRNA and active MMP1 protein levels was upregulated.

conclusionWe found that SMARCD1/MMP-1 is a downstream pathway of hsa-miR-100-5p. hsa-miR-100-5p transfection enhanced the motility of NESCs by inhibiting SMARCD1 expression and MMP1 activation. These findings suggest that enhanced hsa-miR-100-5p expression in endometriosis is involved in promoting the acquisition of endometriosis-specific characteristics during endometriosis development. Our present findings on the roles of hsa-miR-100-5p may thus contribute to understand the epigenetic mechanisms involved in the pathogenesis of endometriosis.

Indexed as

Gene Expression RegulationAdultCell MovementCells, CulturedChromosomal Proteins, Non-HistoneEndometriosisEndometriumFemaleGene Expression ProfilingHumansMatrix Metalloproteinase 1MicroRNAsOvarySignal TransductionStromal CellsYoung AdultChromosomal Proteins, Non-HistoneMatrix Metalloproteinase 1MicroRNAsMIRN100 microRNA, humanSMARCD1 protein, humanEndometriosisHsa-miR-100-5pInvasionMatrix metallopeptidase 1SMARCD1

Identifiers

PMID32299427
PMCPMC7161200
OpenAlexW3016540244

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.