Evidence map›Paper›PMID 37131239›Full record

ArticleJournal of experimental & clinical cancer research : CR2023

miR-92a-1-5p enriched prostate cancer extracellular vesicles regulate osteoclast function via MAPK1 and FoxO1.

Lijuan Yu, Bingdong Sui, Xin Zhang, Jiayun Liu, Xiaoke Hao, Lei Zheng

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2023. 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
2.8field-weighted citation impact, top 10% 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, 18 citations in OpenAlex.

  1. Inhibitory Effect ofInternational journal of nanomedicine · 2026
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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 4 institutions in 2 countries.

Lijuan YuDepartment of Laboratory Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China. lijuan.yu@gu.se.ORCID http://orcid.org/0000-0003-3558-3800
Bingdong SuiResearch and Development Center for Tissue Engineering, School of Stomatology, Fourth Military Medical University (Air Force Medical University), Xi'an, 710032, China.
Xin ZhangDepartment of Laboratory Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Jiayun LiuInstitute of Laboratory Medicine Center of Chinese People's Liberation Army (PLA), Xijing Hospital, Fourth Military Medical University (Air Force Medical University), , Xi'an, 710032, China.
Xiaoke HaoInstitute of Laboratory Medicine Center of Chinese People's Liberation Army (PLA), Xijing Hospital, Fourth Military Medical University (Air Force Medical University), , Xi'an, 710032, China. haoxkg59@163.com.
Lei ZhengDepartment of Laboratory Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China. nfyyzhenglei@smu.edu.cn.
Nanfang Hospital · CNAir Force Medical University · CNNorthwest University · CNXijing Hospital · CN

Funding

National Key R&D Program of China 2021YFA1300604National Natural Science Foundation of China 81872347National Natural Science Foundation of China 82203711National Science Fund for Distinguished Young Scholars 82025024Postdoctoral Research Foundation of China 2021M701631
6 · The paper itself

Abstract

backgroundWe have previously reported that extracellular vesicles (EVs) derived from osteoblastic, osteoclastic and mixed prostate cancer cells promote osteoclast differentiation and inhibit osteoblast differentiation via transferring miR-92a-1-5p. In the present study, we focused on engineering miR-92a-1-5p into EVs and determining any therapeutic roles and mechanisms of the engineered EVs.

methodsA stable prostate cancer cell line (MDA PCa 2b) overexpressing miR-92a-1-5p was constructed by lentivirus, and EVs were isolated by ultracentrifugation. The overexpression of miR-92a-1-5p in both cells and EVs was tested using qPCR. Osteoclast function was evaluated by Trap staining, mRNA expression of osteoclastic markers ctsk and trap, immunolabeling of CTSK and TRAP and microCT using either in vitro and in vivo assays. Target gene of miR-92a-1-5p was proved by a dual-luciferase reporter assay system. siRNAs were designed and used for transient expression in order to determine the role of downstream genes on osteoclast differentiation.

resultsStable overexpression cells of miRNA-92a-5p was associated with EVs upregulating this microRNA, as confirmed by qPCR. Further, miR-92a-1-5p enriched EVs promote osteoclast differentiation in vitro by reducing MAPK1 and FoxO1 expression, associated with increased osteoclast function as shown by TRAP staining and mRNA expression of osteoclast functional genes. siRNA targeting MAPK1 or FoxO1 resulted in similar increase in osteoclast function. In vivo, the miR-92a-1-5p enriched EVs given via i.v. injection promote osteolysis, which was associated with reduction of MAPK1 and FoxO1 expression in bone marrow.

conclusionThese experiments suggest that miR-92a-1-5p enriched EVs regulate osteoclast function via reduction of MAPK1 and FoxO1.

Indexed as

Extracellular VesiclesMicroRNAsProstatic NeoplasmsForkhead Box Protein O1HumansMaleMitogen-Activated Protein Kinase 1OsteoclastsRNA, MessengerForkhead Box Protein O1FOXO1 protein, humanMAPK1 protein, humanMicroRNAsMIRN92 microRNA, humanMitogen-Activated Protein Kinase 1RNA, MessengerBone diseasesBone metabolismmiR-92a-1-5pmiR-92a-1-5p enriched EVsOsteoclast differentiation

Identifiers

PMID37131239
PMCPMC10152631
OpenAlexW4367679161

What OpenQuestion holds

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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.