Evidence map›Paper›PMID 31964905›Full record

ArticleScientific reports2020

Investigating Chaperonin-Containing TCP-1 subunit 2 as an essential component of the chaperonin complex for tumorigenesis.

Anne E Showalter, Ana C Martini, Daniel Nierenberg, Kristen Hosang, Naima Ahmed Fahmi, Priya Gopalan, Amr S Khaled, Wei Zhang, Annette R Khaled

Abstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
–field-weighted citation impact
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

33 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Chaperonin in health and disease.Molecular biomedicine · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. iScience · 2023
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

9 authors.

Anne E Showalter *Division of Cancer Research, Burnett School of Biomedical Science, College of Medicine, University of Central Florida, Orlando, FL, 32827, USA.
Ana C Martini *Division of Cancer Research, Burnett School of Biomedical Science, College of Medicine, University of Central Florida, Orlando, FL, 32827, USA.
Daniel NierenbergDivision of Cancer Research, Burnett School of Biomedical Science, College of Medicine, University of Central Florida, Orlando, FL, 32827, USA.
Kristen HosangDivision of Cancer Research, Burnett School of Biomedical Science, College of Medicine, University of Central Florida, Orlando, FL, 32827, USA.
Naima Ahmed FahmiDepartment of Computer Science, University of Central Florida, Orlando, FL, 32827, USA.
Priya GopalanOncology, Department of Internal Medicine, Orlando VA Medical Center, Orlando, FL, 32827, USA.
Amr S KhaledPathology and Laboratory Medicine, Orlando VA Medical Center, Orlando, FL, 32827, USA.
Wei ZhangDepartment of Computer Science, University of Central Florida, Orlando, FL, 32827, USA.ORCID http://orcid.org/0000-0003-3605-9373
Annette R KhaledDivision of Cancer Research, Burnett School of Biomedical Science, College of Medicine, University of Central Florida, Orlando, FL, 32827, USA. annette.khaled@ucf.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chaperonin-containing TCP-1 (CCT or TRiC) is a multi-subunit complex that folds many of the proteins essential for cancer development. CCT is expressed in diverse cancers and could be an ideal therapeutic target if not for the fact that the complex is encoded by eight distinct genes, complicating the development of inhibitors. Few definitive studies addressed the role of specific subunits in promoting the chaperonin's function in cancer. To this end, we investigated the activity of CCT2 (CCTβ) by overexpressing or depleting the subunit in breast epithelial and breast cancer cells. We found that increasing total CCT2 in cells by 1.3-1.8-fold using a lentiviral system, also caused CCT3, CCT4, and CCT5 levels to increase. Likewise, silencing cct2 gene expression by ~50% caused other CCT subunits to decrease. Cells expressing CCT2 were more invasive and had a higher proliferative index. CCT2 depletion in a syngeneic murine model of triple negative breast cancer (TNBC) prevented tumor growth. These results indicate that the CCT2 subunit is integral to the activity of the chaperonin and is needed for tumorigenesis. Hence CCT2 could be a viable target for therapeutic development in breast and other cancers.

Indexed as

AnimalsBreast NeoplasmsCarcinogenesisCell Line, TumorCell ProliferationChaperonin Containing TCP-1FemaleGene Expression Regulation, NeoplasticHumansKaplan-Meier EstimateMice, Inbred C57BLTriple Negative Breast NeoplasmsXenograft Model Antitumor AssaysCCT2 protein, humanChaperonin Containing TCP-1

Identifiers

PMID31964905
PMCPMC6972895

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.