Evidence map›Paper›PMID 41721921›Full record

ArticleJournal of molecular histology2026

miR-34c-3p promotes osteogenic differentiation of BMSCs by inhibiting DCBLD2 activation of the PI3K/AKT signaling pathway.

Yongcheng Deng, Yihao Lei, Yi Ou, Junnan Li, Xingxi Hu, Lei Wen, Kaiyu Hou

Abstract read
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In one paragraph

Article in Journal of molecular histology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

7 authors.

Yongcheng DengOpthopaedic Trauma Surgery, Affiliation Hospital of Yunnan University, Kunming, 650031, China.
Yihao LeiOpthopaedic Trauma Surgery, Affiliation Hospital of Yunnan University, Kunming, 650031, China.
Yi OuOpthopaedic Trauma Surgery, Affiliation Hospital of Yunnan University, Kunming, 650031, China.
Junnan LiOpthopaedic Trauma Surgery, Affiliation Hospital of Yunnan University, Kunming, 650031, China.
Xingxi HuOpthopaedic Trauma Surgery, Affiliation Hospital of Yunnan University, Kunming, 650031, China.
Lei WenOpthopaedic Trauma Surgery, Affiliation Hospital of Yunnan University, Kunming, 650031, China.
Kaiyu HouOpthopaedic Trauma Surgery, Affiliation Hospital of Yunnan University, Kunming, 650031, China. Wlchmm1971@163.com.

Funding

Yunnan Provincial Department of Science and Technology-Kunming Medical University Joint Special Fund Project 2019FE001(-254)
6 · The paper itself

Abstract

In the process of bone metabolism, osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) is closely related to bone formation, remodeling and repair. As a type I transmembrane protein, DCBLD2 regulates relapsing polychondritis, but its function in the osteogenic differentiation of BMSCs remains unclear. This study aimed to investigate the effects of DCBLD2 on osteogenic differentiation in BMSCs and the underlying regulatory mechanism. Human mesenchymal stem cell osteogenic differentiation medium was used to induce the differentiation of BMSCs into osteoblasts. Osteogenic differentiation of the BMSCs was detected via ALP staining and alizarin red staining, and related genes and proteins were identified via bioinformatics analysis, RT‒qPCR and Western blotting. The binding of miR-34c-3p to DCBLD2 was detected via AGO2-RIP and dual-luciferase reporter gene experiments. This study revealed that DCBLD2 expression is downregulated during osteogenic differentiation of BMSCs. Overexpression of DCBLD2 inhibited the differentiation activity and mineralization of BMSCs while decreasing the expression of OCN, OPN, Runx2, and collagen I and ultimately inhibited the osteogenic differentiation of BMSCs. In addition, the phosphorylation levels of PI3K and AKT increased during osteogenic differentiation of BMSCs, and the PI3K activator 740 Y-P effectively reversed the inhibitory effect of DCBLD2 overexpression on BMSCs osteogenic differentiation. Conversely, miR-34c-3p expression is also upregulated during BMSCs osteogenic differentiation, and miR-34c-3p has a targeted binding relationship with DCBLD2. Knocking down DCBLD2 expression partially weakened the effect of the miR-34c-3p inhibitor and promoted the differentiation of BMSCs. In concludion, miR-34c-3p activates the PI3K/AKT signaling pathway by inhibiting the expression of DCBLD2, thereby promoting osteogenic differentiation of BMSCs.

Indexed as

Cell DifferentiationMesenchymal Stem CellsMicroRNAsOsteogenesisPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionCells, CulturedHumansMicroRNAsMIRN34 microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktBone marrow mesenchymal stem cellsDCBLD2miR-34c-3pOsteogenic differentiationPI3K/AKT signaling pathway

Identifiers

PMID41721921

What Socratic holds

Textmetadata
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 Socratic graph.