Evidence map›Paper›PMID 19838216›Full record

ArticleOncogene2010

Knockdown of protein tyrosine phosphatase SHP-1 inhibits G1/S progression in prostate cancer cells through the regulation of components of the cell-cycle machinery.

F J Rodríguez-Ubreva, A E Cariaga-Martinez, M A Cortés, M Romero-De Pablos, S Ropero, P López-Ruiz, B Colás

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

21 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. Overlapping action of TFrontiers in endocrinology · 2024
    Article
  4. Consideration of SHP-1 as a Molecular Target for Tumor Therapy.International journal of molecular sciences · 2023
    Review
  5. Article
  6. Predicting patient response with models trained on cell lines and patient-derived xenografts by nonlinear transfer learning.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  7. Protein Tyrosine Phosphatases: Mechanisms in Cancer.International journal of molecular sciences · 2021
    Review
  8. Shp1 in Solid Cancers and Their Therapy.Frontiers in oncology · 2020
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. PTPN6 expression is epigenetically regulated and influences survival and response to chemotherapy in high-grade gliomas.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
  16. Article
  17. Review
  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

7 authors at 1 institution in 1 country.

F J Rodríguez-UbrevaDepartamento de Bioquímica y Biología Molecular, Universidad de Alcalá, Alcalá de Henares, E-28871 Madrid, Spain.
A E Cariaga-Martinez
M A Cortés
M Romero-De Pablos
S Ropero
P López-Ruiz
B Colás
Universidad de Alcalá · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SHP-1, a haematopoietic cell-specific tyrosine phosphatase, is also expressed in human prostate. In this study, we report that SHP-1 depletion in PC-3 cells induced by small interfering RNAs causes G1 phase cell-cycle arrest accompanied by changes in some components of the cell-cycle machinery. SHP-1 knockdown increases p27(Kip1) (p27) protein stability, its nuclear localization and p27 gene transcription. These effects could be mediated by PI3K-AKT pathway as SHP-1 interacts with PI3K regulating its activity and p110 catalytic subunit phosphorylation. The increase in p27 protein stability could also because of reduced cyclin-dependent kinase (CDK2) activity. SHP-1 knockdown decreases the CDK6 levels, inducing retinoblastoma protein hypophosphorylation, downregulation of cyclin E and thereby a decrease in the CDK2 activity. However, the codepletion of SHP-1 and p27 does not produce re-entry into the cycle, implying that p27 is not required to maintain cell-cycle arrest induced by SHP-1 depletion. The maintenance of the PC-3 cell anti-proliferative response after p27 loss could be because of mislocalization of CDK2 induced by SHP-1 knockdown. This study shows that SHP-1 depletion promotes cell-cycle arrest by modulating the activity of cell-cycle regulators and suggests that SHP-1 may be required for the proper functioning of events governing cell-cycle progression.

Indexed as

RNA InterferenceBlotting, WesternCell CycleCell Cycle ProteinsCell Line, TumorCell NucleusCell ProliferationCyclin-Dependent Kinase 2Cyclin-Dependent Kinase 6Cyclin-Dependent Kinase Inhibitor p27Cyclin EG1 PhaseGene Expression Regulation, NeoplasticHumansLuciferasesMaleCDK2 protein, humanCDK6 protein, humanCell Cycle ProteinsCyclin-Dependent Kinase 2Cyclin-Dependent Kinase 6Cyclin-Dependent Kinase Inhibitor p27Cyclin ELuciferasesProtein Tyrosine Phosphatase, Non-Receptor Type 6PTPN6 protein, humanRetinoblastoma Protein

Identifiers

PMID19838216
OpenAlexW2039319602

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.