Evidence map›Paper›PMID 23115191›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012

Tis21 knock-out enhances the frequency of medulloblastoma in Patched1 heterozygous mice by inhibiting the Cxcl3-dependent migration of cerebellar neurons.

Stefano Farioli-Vecchioli, Irene Cinà, Manuela Ceccarelli, Laura Micheli, Luca Leonardi, Maria Teresa Ciotti, Marco De Bardi, Concezio Di Rocco, Roberto Pallini, Sebastiano Cavallaro and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

37 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
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  9. Review
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  11. Review
  12. Article
  13. CXCL3 Signaling in the Tumor Microenvironment.Advances in experimental medicine and biology · 2021
    Review
  14. Article
  15. Article
  16. Review
  17. The Non-coding Side of Medulloblastoma.Frontiers in cell and developmental biology · 2020
    Review
  18. Article
  19. Tumor suppressors BTG1 and BTG2: Beyond growth control.Journal of cellular physiology · 2019
    Review
  20. Article
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.

Stefano Farioli-VecchioliInstitute of Cell Biology and Neurobiology, National Research Council, Fondazione Santa Lucia, 00143 Rome, Italy.
Irene Cinà
Manuela Ceccarelli
Laura Micheli
Luca Leonardi
Maria Teresa Ciotti
Marco De Bardi
Concezio Di Rocco
Roberto Pallini
Sebastiano Cavallaro
Felice Tirone
Institute of Cell Biology and Neurobiology · ITFondazione Santa Lucia · ITUniversità Cattolica del Sacro Cuore · ITNational Academies of Sciences, Engineering, and Medicine · USNational Research Council · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A failure in the control of proliferation of cerebellar granule neuron precursor cells (GCPs), located in the external granular layer (EGL) of the cerebellum, gives rise to medulloblastoma. To investigate the process of neoplastic transformation of GCPs, we generated a new medulloblastoma model by crossing Patched1 heterozygous mice, which develop medulloblastomas with low frequency, with mice lacking the Tis21 gene. Overexpression of Tis21 is known to inhibit proliferation and trigger differentiation of GCPs; its expression decreases in human medulloblastomas. Double-knock-out mice show a striking increase in the frequency of medulloblastomas and hyperplastic EGL lesions, formed by preneoplastic GCPs. Tis21 deletion does not affect the proliferation of GCPs but inhibits their differentiation and, chiefly, their intrinsic ability to migrate outside the EGL. This defect of migration may represent an important step in medulloblastoma formation, as GCPs, remaining longer in the EGL proliferative niche, may become more prone to transformation. By genome-wide analysis, we identified the chemokine Cxcl3 as a target of Tis21. Cxcl3 is downregulated in Tis21-null GCPs of EGL and lesions; addition of Cxcl3 to cerebellar slices rescues the defective migration of Tis21-null GCPs and, remarkably, reduces the area of hyperplastic lesions. As Tis21 activates Cxcl3 transcription, our results suggest that Tis21 induces migration of GCPs through Cxcl3, which may represent a novel target for medulloblastoma therapy.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsBromodeoxyuridineCell CountCell MovementCell ProliferationCerebellar NeoplasmsCerebellumChemokines, CXCGenetic VectorsGenotypeHeterozygoteImmediate-Early ProteinsImmunohistochemistryImmunoprecipitationIn Situ HybridizationAtoh1 protein, mouseBasic Helix-Loop-Helix ProteinsBromodeoxyuridineBtg2 protein, mouseChemokines, CXCCxcl3 protein, mouseImmediate-Early ProteinsPatched-1 ReceptorPatched ReceptorsPTCH1 protein, humanPtch1 protein, mouseReceptors, Cell SurfaceTumor Suppressor Proteins

Identifiers

PMID23115191
PMCPMC6621585
OpenAlexW1973164032

What OpenQuestion 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 OpenQuestion graph.