Evidence map›Paper›PMID 26775693›Full record

ReviewCell death & disease2016

P53 functional abnormality in mesenchymal stem cells promotes osteosarcoma development.

T Velletri, N Xie, Y Wang, Y Huang, Q Yang, X Chen, Q Chen, P Shou, Y Gan, G Cao and 2 more

Open access · goldAbstract readReview
In one paragraph

Review in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
9.2field-weighted citation impact, top 2% 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

62 citing papers in PubMed, 91 citations in OpenAlex.

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  11. Potential of Gut Microbial Metabolites in Treating Osteoporosis and Obesity: A Network Pharmacology and Bioinformatics Approach.Medical science monitor : international medical journal of experimental and clinical research · 2024
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2 more citing papers are in PubMed but not listed here.

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

12 authors at 3 institutions in 3 countries.

T VelletriKey Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences/Shanghai Jiao Tong University, School of Medicine, 320 Yueyang Road, Shanghai 200031, China.
N XieKey Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences/Shanghai Jiao Tong University, School of Medicine, 320 Yueyang Road, Shanghai 200031, China.
Y WangKey Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences/Shanghai Jiao Tong University, School of Medicine, 320 Yueyang Road, Shanghai 200031, China.
Y HuangKey Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences/Shanghai Jiao Tong University, School of Medicine, 320 Yueyang Road, Shanghai 200031, China.
Q YangKey Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences/Shanghai Jiao Tong University, School of Medicine, 320 Yueyang Road, Shanghai 200031, China.
X ChenKey Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences/Shanghai Jiao Tong University, School of Medicine, 320 Yueyang Road, Shanghai 200031, China.
Q ChenKey Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences/Shanghai Jiao Tong University, School of Medicine, 320 Yueyang Road, Shanghai 200031, China.
P ShouKey Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences/Shanghai Jiao Tong University, School of Medicine, 320 Yueyang Road, Shanghai 200031, China.ORCID http://orcid.org/0000-0001-7685-7471
Y GanKey Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences/Shanghai Jiao Tong University, School of Medicine, 320 Yueyang Road, Shanghai 200031, China.
G CaoKey Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences/Shanghai Jiao Tong University, School of Medicine, 320 Yueyang Road, Shanghai 200031, China.
G MelinoBiochemistry Laboratory IDI-IRCC, Department of Experimental Medicine and Surgery, University of Rome Torvergata, Rome 00133, Italy.
Y ShiKey Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences/Shanghai Jiao Tong University, School of Medicine, 320 Yueyang Road, Shanghai 200031, China.
Shanghai Jiao Tong University · CNUniversity of Rome Tor Vergata · ITSoochow University · CN

Funding

Medical Research Council MC_U132670600
6 · The paper itself

Abstract

It has been shown that p53 has a critical role in the differentiation and functionality of various multipotent progenitor cells. P53 mutations can lead to genome instability and subsequent functional alterations and aberrant transformation of mesenchymal stem cells (MSCs). The significance of p53 in safeguarding our body from developing osteosarcoma (OS) is well recognized. During bone remodeling, p53 has a key role in negatively regulating key factors orchestrating the early stages of osteogenic differentiation of MSCs. Interestingly, changes in the p53 status can compromise bone homeostasis and affect the tumor microenvironment. This review aims to provide a unique opportunity to study the p53 function in MSCs and OS. In the context of loss of function of p53, we provide a model for two sources of OS: MSCs as progenitor cells of osteoblasts and bone tumor microenvironment components. Standing at the bone remodeling point of view, in this review we will first explain the determinant function of p53 in OS development. We will then summarize the role of p53 in monitoring MSC fidelity and in regulating MSC differentiation programs during osteogenesis. Finally, we will discuss the importance of loss of p53 function in tissue microenvironment. We expect that the information provided herein could lead to better understanding and treatment of OS.

Indexed as

Bone NeoplasmsCell DifferentiationCells, CulturedGenes, p53HumansMesenchymal Stem CellsOsteosarcoma

Identifiers

PMID26775693
PMCPMC4816167
OpenAlexW2342619391

What Socratic holds

Textmetadata
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 Socratic graph.