Evidence map›Paper›PMID 32316593›Full record

ArticleCancers2020

Depletion of Trichoplein (TpMs) Causes Chromosome Mis-Segregation, DNA Damage and Chromosome Instability in Cancer Cells.

Angela Lauriola, Andrea Martello, Sebastian Fantini, Gaetano Marverti, Tommaso Zanocco-Marani, Pierpaola Davalli, Daniele Guardavaccaro, Sabine Mai, Andrea Caporali, Domenico D'Arca

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 36% 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

6 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. The emerging role of the KCTD proteins in cancer.Cell communication and signaling : CCS · 2021
    Review
  6. 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 4 institutions in 3 countries.

Angela LauriolaDepartment of Biomedical, Metabolic and Neural Sciences, Via G. Campi 287, University of Modena and Reggio Emilia, 41125 Modena, Italy.ORCID 0000-0001-5286-8627
Andrea MartelloUniversity/British Heart Foundation Centre for Cardiovascular Science, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh EH16 4TJ, UK.
Sebastian FantiniDepartment of Life Sciences, Via G. Campi 213/d, University of Modena and Reggio Emilia, 41125 Modena, Italy.
Gaetano MarvertiDepartment of Biomedical, Metabolic and Neural Sciences, Via G. Campi 287, University of Modena and Reggio Emilia, 41125 Modena, Italy.ORCID 0000-0002-9074-0795
Tommaso Zanocco-MaraniDepartment of Life Sciences, Via G. Campi 213/d, University of Modena and Reggio Emilia, 41125 Modena, Italy.ORCID 0000-0002-9911-7078
Pierpaola DavalliDepartment of Biomedical, Metabolic and Neural Sciences, Via G. Campi 287, University of Modena and Reggio Emilia, 41125 Modena, Italy.
Daniele GuardavaccaroDepartment of Biotechnology, University of Verona, 37134 Verona, Italy.
Sabine MaiCell Biology, Research Institute of Oncology and Hematology, University of Manitoba, CancerCare Manitoba, Winnipeg, MB R3E 0V9, Canada.ORCID 0000-0002-5797-2201
Andrea CaporaliUniversity/British Heart Foundation Centre for Cardiovascular Science, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh EH16 4TJ, UK.ORCID 0000-0003-2905-3096
Domenico D'ArcaDepartment of Biomedical, Metabolic and Neural Sciences, Via G. Campi 287, University of Modena and Reggio Emilia, 41125 Modena, Italy.ORCID 0000-0002-7240-6005
University of Modena and Reggio Emilia · ITBritish Heart Foundation · GBUniversity of Verona · ITCancerCare Manitoba · CA

Funding

British Heart Foundation FS/11/52/29018British Heart Foundation FS/11/52/29018; MR/R014353/1; FS/14/7/30574British Heart Foundation FS/14/7/30574CIHR CIHRMedical Research Council MR/R014353/1
6 · The paper itself

Abstract

Mitotic perturbations frequently lead to chromosome mis-segregation that generates genome instability, thereby triggering tumor onset and/or progression. Error-free mitosis depends on fidelity-monitoring systems that ensure the temporal and spatial coordination of chromosome segregation. Recent investigations are focused on mitotic DNA damage response (DDR) and chromosome mis-segregations with the aim of developing more efficient anti-cancer therapies. We previously demonstrated that trichoplein keratin filament binding protein (TpMs) exhibits hallmarks of a tumor suppressor gene in cancer-derived cells and human tumors. Here, we show that silencing of TpMs expression results in chromosome mis-segregation, DNA damage and chromosomal instability. TpMs interacts with Mad2, and TpMs depletion results in decreased levels of Mad2 and Cyclin B1 proteins. All the genetic alterations observed are consistent with both defective activation of the spindle assembly checkpoint and mitotic progression. Thus, low levels of TpMs found in certain human tumors may contribute to cellular transformation by promoting genomic instability.

Indexed as

cancerchromosome instability (CIN)chromosome mis-segregationDNA damageMad2mitostatinspectral karyotyping (SKY)spindle assembly checkpoint (SAC)

Identifiers

PMID32316593
PMCPMC7226535
OpenAlexW3016724706

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.