Evidence map›Paper›PMID 26280018›Full record

ArticleDiscoveries (Craiova, Romania)

PLK1 is a binding partner and a negative regulator of FOXO3 tumor suppressor.

Octavian Bucur, Andreea Lucia Stancu, Maria Sinziana Muraru, Armelle Melet, Stefana Maria Petrescu, Roya Khosravi-Far

Open access · hybridAbstract read
In one paragraph

Article in Discoveries (Craiova, Romania). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

20 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Apoptosis regulation by the tyrosine-protein kinase CSK.Frontiers in cell and developmental biology · 2022
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. PLK1, A Potential Target for Cancer Therapy.Translational oncology · 2017
    Review
  18. microRNA regulators of apoptosis in cancer.Discoveries (Craiova, Romania) · 2016
    Review
  19. Article
  20. 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

6 authors at 3 institutions in 3 countries.

Octavian BucurDepartment of Pathology, Harvard Medical School and Beth Israel Deaconess Medical Center, Boston, MA, USA ; Institute of Biochemistry of the Romanian Academy, Bucharest, Romania.
Andreea Lucia StancuDepartment of Pathology, Harvard Medical School and Beth Israel Deaconess Medical Center, Boston, MA, USA.
Maria Sinziana MuraruDepartment of Pathology, Harvard Medical School and Beth Israel Deaconess Medical Center, Boston, MA, USA.
Armelle MeletUniversity Paris Descartes, Paris, France.
Stefana Maria PetrescuInstitute of Biochemistry of the Romanian Academy, Bucharest, Romania.
Roya Khosravi-FarDepartment of Pathology, Harvard Medical School and Beth Israel Deaconess Medical Center, Boston, MA, USA ; Biological and Biomedical Sciences Program, Harvard Medical School, Boston, MA, USA.
Beth Israel Deaconess Medical Center · USRomanian Academy · ROUniversité Paris Cité · FR

Funding

Tumor Selective Apoptosis by TRAILR01HL080192 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KHOSRAVI-FAR, ROYA · 2005 to 2010
$3.6M
Novel Strategies for Treatment of Myeloproliferative DisordersR01CA131664 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KHOSRAVI-FAR, ROYA · 2008 to 2012
$1.8M
Oncogene-Induced Evasion from ApoptosisR01CA105306 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KHOSRAVI-FAR, ROYA · 2005 to 2009
$1.6M
NCI NIH HHS R01 CA105306NCI NIH HHS R01 CA131664NHLBI NIH HHS R01 HL080192
6 · The paper itself

Abstract

FOXO family members (FOXOs: FOXO1, FOXO3, FOXO4 and FOXO6) are important transcription factors and tumor suppressors controlling cell homeostasis and cell fate. They are characterized by an extraordinary functional diversity, being involved in regulation of cell cycle, proliferation, apoptosis, DNA damage response, oxidative detoxification, cell differentiation and stem cell maintenance, cell metabolism, angiogenesis, cardiac and other organ's development, aging, and other critical cellular processes. FOXOs are tightly regulated by reversible phosphorylation, ubiquitination, acetylation and methylation. Interestingly, the known kinases phosphorylate only a small percentage of the known or predicted FOXOs phosphorylation sites, suggesting that additional kinases that phosphorylate and control FOXOs activity exist. In order to identify novel regulators of FOXO3, we have employed a proteomics screening strategy. Using HeLa cancer cell line and a Tandem Affinity Purification followed by Mass Spectrometry analysis, we identified several proteins as binding partners of FOXO3. Noteworthy, Polo Like Kinase 1 (PLK1) proto-oncogene was one of the identified FOXO3 binding partners. PLK1 plays a critical role during cell cycle (G2-M transition and all phases of mitosis) and in maintenance of genomic stability. Our experimental results presented in this manuscript demonstrate that FOXO3 and PLK1 exist in a molecular complex through most of the phases of the cell cycle, with a higher occurrence in the G2-M cell cycle phases. PLK1 induces translocation of FOXO3 from the nucleus to the cytoplasm and suppresses FOXO3 activity, measured by the decrease in the pro-apoptotic Bim protein levels and in the cell cycle inhibitor protein p27. Furthermore, PLK1 can directly phosphorylate FOXO3 in an

Indexed as

apoptosiscell cycleFOXO1FOXO3 binding partnersFOXO tumor suppressorsPI3K-Akt pathwayPolo Like Kinase 1proto-oncogenetranscription factors

Identifiers

PMID26280018
PMCPMC4535815
OpenAlexW2096245692

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.