Evidence map›Paper›PMID 36980704›Full record

ArticleCancers2023

Endothelial Progenitor Cells Promote Osteosarcoma Progression and Invasiveness via AKT/PI3K Signaling.

Ofri Doppelt-Flikshtain, Amin Younis, Tal Tamari, Ofir Ginesin, Talia Shentzer-Kutiel, David Nikomarov, Gil Bar-Sela, Benjamin R Coyac, Yehuda G Assaraf, Hadar Zigdon-Giladi

Open access · goldFull text read
In one paragraph

Article in Cancers, 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
1.7field-weighted citation impact, top 16% 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, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Endothelial progenitor cells in pregnancy-related diseases.Clinical science (London, England : 1979) · 2023
    Review
  9. Deciphering the Signaling Mechanisms of Osteosarcoma Tumorigenesis.International journal of molecular sciences · 2023
    Review
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

10 authors at 2 institutions in 1 country.

Ofri Doppelt-FlikshtainLaboratory for Bone Repair, Rambam Health Care Campus, Haifa 3109601, Israel.
Amin YounisLaboratory for Bone Repair, Rambam Health Care Campus, Haifa 3109601, Israel.
Tal TamariLaboratory for Bone Repair, Rambam Health Care Campus, Haifa 3109601, Israel.
Ofir GinesinLaboratory for Bone Repair, Rambam Health Care Campus, Haifa 3109601, Israel.ORCID 0000-0002-8736-9753
Talia Shentzer-KutielThoracic Cancer Service, Rambam Health Campus, Haifa 3109601, Israel.
David NikomarovMusculoskeletal Oncology Department, Rambam Health Campus, Haifa 3109601, Israel.ORCID 0000-0001-5552-2496
Gil Bar-SelaThe Ruth and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa 3525422, Israel.
Benjamin R CoyacLaboratory for Bone Repair, Rambam Health Care Campus, Haifa 3109601, Israel.
Yehuda G AssarafThe Fred Wyszkowski Cancer Research Laboratory, Department of Biology, Technion-Israel Institute of Technology, Haifa 3200003, Israel.
Hadar Zigdon-GiladiLaboratory for Bone Repair, Rambam Health Care Campus, Haifa 3109601, Israel.ORCID 0000-0002-4940-6533
Technion – Israel Institute of Technology · ILRambam Health Care Campus · IL

Funding

Israel Cancer Association 20200122The Rappaport Institute, Rappaport Faculty of Medicine, Technion, Haifa, Israel NA
6 · The paper itself

Abstract

backgroundOsteosarcoma (OS) mortality is attributed to lung metastases. Endothelial progenitor cells (EPCs) mediate the angiogenic switch in several cancers. The spatial proximity between EPCs and OS in the bone led to the hypothesis that EPCs-osteosarcoma interactions may possibly promote OS progression and aggressiveness.

methodsA PI3K inhibitor, Bevacizumab (an anti-VEGF-A antibody), and an anti-FGF2 antibody were added to the EPCs' conditioned medium (EPC-CM), and their impacts on OS cell (U2-OS and 143B) proliferation, migration, invasion, MMP9 expression, and AKT phosphorylation were determined. The autocrine role of VEGF-A was assessed using Bevacizumab treatment and VEGF-A silencing in OS cells. Toward this end, an orthotopic mouse OS model was established. Mouse and human tumors were immunolabeled with antibodies to the abovementioned factors.

resultsEPC-CM enhanced osteosarcoma MMP9 expression, invasiveness, and migration via the PI3K/AKT pathway. The addition of Bevacizumab and an anti-FGF2 antibody to the EPC-CM diminished OS cell migration. The autocrine role of VEGF-A was assessed using Bevacizumab and VEGF-A silencing in OS cells, resulting in decreased AKT phosphorylation and, consequently, diminished invasiveness and migration. Consistently, OS xenografts in mice displayed high VEGF-A and FGF2 levels. Remarkably, lung metastasis specimens derived from OS patients exhibited marked immunolabeling of CD31, VEGF-A, and FGF2

Indexed as

endothelial progenitor cellsmetastasisosteosarcoma

Identifiers

PMID36980704
PMCPMC10046883
OpenAlexW4327738147

What OpenQuestion holds

Textfull text, public
LicenceCC BY
reference markers read2
measurements read91
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 OpenQuestion graph.