Evidence map›Paper›PMID 40481141›Full record

ArticleScientific reports2025

EIF4A3 enhances the viability, invasion and osteogenic differentiation of BMSCs via the USP53/SMAD5 pathway.

Gang Cheng, Xiaoling Yang, Yongtao Tang, Changjun Wu, Zulin Tang, Siqi Wei

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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.

Gang ChengDepartment of Spinal Surgery, Shenzhen Guangming District People's Hospital, Shenzhen, 518107, China.
Xiaoling YangTangjia Community Health Service Center, University of Chinese Academy of Sciences Shenzhen Hospital, Shenzhen, 518106, China.
Yongtao TangDepartment of Spinal Surgery, University of Chinese Academy of Sciences Shenzhen Hospital, No. 4253 Songbai Road, Matan Street, Guangming District, Shenzhen, 518106, China.
Changjun WuDepartment of Spinal Surgery, University of Chinese Academy of Sciences Shenzhen Hospital, No. 4253 Songbai Road, Matan Street, Guangming District, Shenzhen, 518106, China.
Zulin TangDepartment of Spinal Surgery, University of Chinese Academy of Sciences Shenzhen Hospital, No. 4253 Songbai Road, Matan Street, Guangming District, Shenzhen, 518106, China.
Siqi WeiDepartment of Spinal Surgery, University of Chinese Academy of Sciences Shenzhen Hospital, No. 4253 Songbai Road, Matan Street, Guangming District, Shenzhen, 518106, China. weisiqi72@126.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SMAD5 has been demonstrated to promote osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) through the circ_0001825/miR-1270/SMAD5 axis or KCNQ1OT1/miR-320a/SMAD5 axis. Therefore, SMAD5 may be a key regulator of BMSCs osteogenic differentiation, and its more related molecular mechanisms are worth further revealing. Western blot analysis was used to detect the protein levels of SMAD5, ubiquitin-specific peptidase 53 (USP53), eukaryotic translation initiation factor 4A3 (EIF4A3), and osteogenic differentiation-related markers. Cell counting kit 8 and transwell assay were performed to measure cell viability and invasion. Alkaline phosphatase (ALP) activity detection and Alizarin red S staining were employed to assess osteogenic differentiation. The interactions between USP53 and SMAD5/EIF4A3 were confirmed by Co-immunoprecipitation assay. The mRNA levels of SMAD5 and USP53 were examined using quantitative real-time PCR. SMAD5 silencing suppressed viability, invasion and osteogenic differentiation of BMSCs, while its overexpression had opposite effects. USP53 deubiquitinated SMAD5 to stabilize its protein expression. Moreover, USP53 knockdown inhibited viability, invasion and osteogenic differentiation of BMSCs, while these effects were reverted by SMAD5 overexpression. EIF4A3 stabilized USP53 mRNA expression, and the inhibitory effect of EIF4A3 silencing on viability, invasion and osteogenic differentiation of BMSCs was abolished by USP53 overexpression. Furthermore, EIF4A3 enhanced SMAD5 expression by interacting with USP53. EIF4A3-stabilized USP53 promotes SMAD5 deubiquitination to enhance viability, invasion and osteogenic differentiation of BMSCs.

Indexed as

Cell DifferentiationEukaryotic Initiation Factor-4AMesenchymal Stem CellsOsteogenesisSmad5 ProteinUbiquitin-Specific ProteasesAnimalsCells, CulturedCell SurvivalHumansSignal TransductionEukaryotic Initiation Factor-4ASmad5 ProteinSMAD5 protein, humanUbiquitin-Specific ProteasesBMSCsEIF4A3Osteogenic differentiationSMAD5USP53

Identifiers

PMID40481141
PMCPMC12144208

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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.