Evidence map›Paper›PMID 26616853›Full record

ArticleOncogene2016

CD99 regulates neural differentiation of Ewing sarcoma cells through miR-34a-Notch-mediated control of NF-κB signaling.

S Ventura, D N T Aryee, F Felicetti, A De Feo, C Mancarella, M C Manara, P Picci, M P Colombo, H Kovar, A Carè and 1 more

Abstract read
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
  2. Review
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  15. Article
  16. Identification of Novel/RareInternational journal of molecular sciences · 2024
    Article
  17. Article
  18. Review
  19. Article
  20. Small round cell sarcomas.Nature reviews. Disease primers · 2022
    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

11 authors at 5 institutions in 2 countries.

S VenturaCRS Development of Biomolecular Therapies, Experimental Oncology Laboratory, Rizzoli Istituto Ortopedico, Bologna, Italy.
D N T AryeeChildren's Cancer Research Institute, St Anna Kinderkrebsforschung, Vienna, Austria.
F FelicettiDepartment of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome, Italy.
A De FeoDepartment of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome, Italy.
C MancarellaCRS Development of Biomolecular Therapies, Experimental Oncology Laboratory, Rizzoli Istituto Ortopedico, Bologna, Italy.
M C ManaraCRS Development of Biomolecular Therapies, Experimental Oncology Laboratory, Rizzoli Istituto Ortopedico, Bologna, Italy.
P PicciCRS Development of Biomolecular Therapies, Experimental Oncology Laboratory, Rizzoli Istituto Ortopedico, Bologna, Italy.
M P ColomboMolecular Immunology Unit, Department of Experimental Oncology and Molecular Medicine, Fondazione IRCCS 'Istituto Nazionale dei Tumori', Milan, Italy.
H KovarChildren's Cancer Research Institute, St Anna Kinderkrebsforschung, Vienna, Austria.
A CarèDepartment of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome, Italy.
K ScotlandiCRS Development of Biomolecular Therapies, Experimental Oncology Laboratory, Rizzoli Istituto Ortopedico, Bologna, Italy.
Istituto Ortopedico Rizzoli · ITIstituto Superiore di Sanità · ITFondazione IRCCS Istituto Nazionale dei Tumori · ITSt. Anna Children's Cancer Research InstituteSt Anna Children's Hospital · AT

Funding

Austrian Science Fund FWF P 24708
6 · The paper itself

Abstract

Sarcomas are mesenchymal tumors characterized by blocked differentiation process. In Ewing sarcoma (EWS) both CD99 and EWS-FLI1 concur to oncogenesis and inhibition of differentiation. Here, we demonstrate that uncoupling CD99 from EWS-FLI1 by silencing the former, nuclear factor-κB (NF-κB) signaling is inhibited and the neural differentiation program is re-established. NF-κB inhibition passes through miR-34a-mediated repression of Notch pathway. CD99 counteracts EWS-FLI1 in controlling NF-κB signaling through the miR-34a, which is increased and secreted into exosomes released by CD99-silenced EWS cells. Delivery of exosomes from CD99-silenced cells was sufficient to induce neural differentiation in recipient EWS cells through miR-34a inhibition of Notch-NF-κB signaling. Notably, even the partial delivery of CD99 small interfering RNA may have a broad effect on the entire tumor cell population owing to the spread operated by their miR-34a-enriched exosomes, a feature opening to a new therapeutic option.

Indexed as

12E7 AntigenCell DifferentiationHumansMicroRNAsNF-kappa BOncogene Proteins, FusionProto-Oncogene Protein c-fli-1Receptors, NotchRNA-Binding Protein EWSRNA, Small InterferingSarcoma, EwingSignal Transduction12E7 AntigenCD99 protein, humanEWS-FLI fusion proteinMicroRNAsMIRN34 microRNA, humanNF-kappa BOncogene Proteins, FusionProto-Oncogene Protein c-fli-1Receptors, NotchRNA-Binding Protein EWSRNA, Small Interfering

Identifiers

PMID26616853
PMCPMC4967355
OpenAlexW2411116122

What OpenQuestion holds

Textmetadata
LicenceTDM
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.