Evidence map›Paper›PMID 33922633›Full record

ReviewBiomolecules2021

Centrosome Dynamics and Its Role in Inflammatory Response and Metastatic Process.

Massimo Pancione, Luigi Cerulo, Andrea Remo, Guido Giordano, Álvaro Gutierrez-Uzquiza, Paloma Bragado, Almudena Porras

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.0field-weighted citation impact, top 29% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Chromosomal Instability Drives Glioblastoma Heterogeneity and Therapeutic Opportunities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  2. The roles of centrosome amplification in diabetes-associated diseases.Frontiers in cell and developmental biology · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. 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

7 authors at 3 institutions in 2 countries.

Massimo PancioneDepartment of Sciences and Technologies, University of Sannio, 82100 Benevento, Italy.
Luigi CeruloDepartment of Sciences and Technologies, University of Sannio, 82100 Benevento, Italy.
Andrea RemoPathology Unit, Mater Salutis Hospital AULSS9, "Scaligera", 37122 Verona, Italy.ORCID 0000-0002-2564-2988
Guido GiordanoDepartment of Medical Oncology Unit, University of Foggia, 71122 Foggia, Italy.ORCID 0000-0002-9310-1075
Álvaro Gutierrez-UzquizaDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy, Complutense University Madrid, 28040 Madrid, Spain.
Paloma BragadoDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy, Complutense University Madrid, 28040 Madrid, Spain.
Almudena PorrasDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy, Complutense University Madrid, 28040 Madrid, Spain.ORCID 0000-0002-6495-3308
Universidad Complutense de Madrid · ESUniversity of Sannio · ITUniversity of Foggia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metastasis is a process by which cancer cells escape from the location of the primary tumor invading normal tissues at distant organs. Chromosomal instability (CIN) is a hallmark of human cancer, associated with metastasis and therapeutic resistance. The centrosome plays a major role in organizing the microtubule cytoskeleton in animal cells regulating cellular architecture and cell division. Loss of centrosome integrity activates the p38-p53-p21 pathway, which results in cell-cycle arrest or senescence and acts as a cell-cycle checkpoint pathway. Structural and numerical centrosome abnormalities can lead to aneuploidy and CIN. New findings derived from studies on cancer and rare genetic disorders suggest that centrosome dysfunction alters the cellular microenvironment through Rho GTPases, p38, and JNK (c-Jun N-terminal Kinase)-dependent signaling in a way that is favorable for pro-invasive secretory phenotypes and aneuploidy tolerance. We here review recent data on how centrosomes act as complex molecular platforms for Rho GTPases and p38 MAPK (Mitogen activated kinase) signaling at the crossroads of CIN, cytoskeleton remodeling, and immune evasion via both cell-autonomous and non-autonomous mechanisms.

Indexed as

AneuploidyAnimalsCell CycleCell Cycle CheckpointsCentrosomeChromosomal InstabilityCytoskeletonHumansInflammationJNK Mitogen-Activated Protein KinasesMAP Kinase Signaling SystemMicrotubulesNeoplasm MetastasisNeoplasmsp38 Mitogen-Activated Protein Kinasesrho GTP-Binding ProteinsJNK Mitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein Kinasesrho GTP-Binding ProteinsTumor Suppressor Protein p53centrosomechromosome instabilityp38 MAPKRho GTPasestumor microenvironment

Identifiers

PMID33922633
PMCPMC8146599
OpenAlexW3159799246

What OpenQuestion 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 OpenQuestion graph.