Evidence map›Paper›PMID 42272134›Full record

ArticleCell proliferation2026

Dental Pulp Stem Cell-Derived Intracellular Vesicles Inhibit OSCC by Delivering PTEN to Suppress PI3K/AKT/mTOR Signalling Pathway.

Yu Luo, Qiang Qin, Wenting She, Xiangying Wang, Xiqin Li, Chenxuan Shu, Ruohan Li, Ziwei Li, Dongjie Fu, Yan He and 1 more

Abstract read
In one paragraph

Article in Cell proliferation, 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

11 authors.

Yu LuoCenter of Regenerative Medicine and Department of Stomatology, Renmin Hospital of Wuhan University, Wuhan, China.ORCID https://orcid.org/0000-0002-6653-0376
Qiang QinCenter of Regenerative Medicine and Department of Stomatology, Renmin Hospital of Wuhan University, Wuhan, China.
Wenting SheCenter of Regenerative Medicine and Department of Stomatology, Renmin Hospital of Wuhan University, Wuhan, China.
Xiangying WangCenter of Regenerative Medicine and Department of Stomatology, Renmin Hospital of Wuhan University, Wuhan, China.
Xiqin LiCenter of Regenerative Medicine and Department of Stomatology, Renmin Hospital of Wuhan University, Wuhan, China.
Chenxuan ShuCenter of Regenerative Medicine and Department of Stomatology, Renmin Hospital of Wuhan University, Wuhan, China.
Ruohan LiCenter of Regenerative Medicine and Department of Stomatology, Renmin Hospital of Wuhan University, Wuhan, China.
Ziwei LiCenter of Regenerative Medicine and Department of Stomatology, Renmin Hospital of Wuhan University, Wuhan, China.
Dongjie FuCenter of Regenerative Medicine and Department of Stomatology, Renmin Hospital of Wuhan University, Wuhan, China.ORCID https://orcid.org/0000-0002-6388-9455
Yan HeInstitute of Regenerative and Translational Medicine, Tianyou Hospital, Wuhan University of Science and Technology, Wuhan, China.
Qingsong YeCenter of Regenerative Medicine and Department of Stomatology, Renmin Hospital of Wuhan University, Wuhan, China.

Funding

National Natural Science Foundation of China 82571057State Key Project Ministry of Science and Technology of China 2022YFC2504200
6 · The paper itself

Abstract

Oral squamous cell carcinoma (OSCC) represents a globally predominant type of oral malignancy with escalating incidence, featuring aggressive biological behaviour, prominent metastatic potential and poor clinical outcomes. Emerging evidence positions dental pulp stem cell-sourced intracellular vesicles (DPSC-IVs) as novel therapeutic vectors in regenerative oncology, citing their low immunogenicity, favourable safety profile and ability to modulate tumour microenvironment. In this study, DPSC-IVs significantly inhibited OSCC progression both in vitro and in vivo, suppressing tumour cell proliferation, invasion and colony formation while simultaneously promoting apoptosis. Notably, the antitumor effect of DPSC-IVs was further enhanced by combining them with autophagy inhibitor 3-methyladenine (3-MA), which synergistically suppressed the PI3K/AKT/mTOR pathway and enhanced mitochondrial stress while suppressing residual cytoprotective autophagy. Mechanistically, DPSC-IVs served as carriers of PTEN into OSCC cells, which in turn suppressed oncogenic PI3K/AKT signalling and induced excessive mitophagy. Taken together, this study indicated that DPSC-IVs could suppress OSCC through dual mechanisms, highlighting their potential as a promising and clinically translatable therapeutic option with advantages in safety and scalable production.

Indexed as

DPSC‐IVsOSCCPI3K/AKT/mTOR signalling pathwayPINK1/parkin mediated mitophagy

Identifiers

PMID42272134
PMCPMC13326028

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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.