Evidence map›Paper›PMID 26934321›Full record

ArticleOncotarget2016

Class II phosphoinositide 3-kinase C2β regulates a novel signaling pathway involved in breast cancer progression.

Anissa Chikh, Riccardo Ferro, Jonathan J Abbott, Roberto Piñeiro, Richard Buus, Manuela Iezzi, Francesca Ricci, Daniele Bergamaschi, Paola Ostano, Giovanna Chiorino and 5 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. 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
1.4field-weighted citation impact, top 18% 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, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Exploring the Therapeutic Potential ofInternational journal of molecular sciences · 2023
    Article
  6. Review
  7. Review
  8. Design, synthesis, and biological evaluation of new thieno[2,3-Journal of enzyme inhibition and medicinal chemistry · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. An Overview of Class II Phosphoinositide 3-Kinases.Current topics in microbiology and immunology · 2022
    Article
  14. Article
  15. Review
  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

15 authors at 5 institutions in 3 countries.

Anissa ChikhQueen Mary University of London, Barts and The London School of Medicine and Dentistry, Blizard Institute, Centre for Cell Biology and Cutaneous Research, London, UK.
Riccardo FerroQueen Mary University of London, Barts and The London School of Medicine and Dentistry, Blizard Institute, Centre for Cell Biology and Cutaneous Research, London, UK.
Jonathan J AbbottQueen Mary University of London, Barts and The London School of Medicine and Dentistry, Blizard Institute, Centre for Cell Biology and Cutaneous Research, London, UK.
Roberto PiñeiroQueen Mary University of London, Barts and The London School of Medicine and Dentistry, Blizard Institute, Centre for Cell Biology and Cutaneous Research, London, UK.
Richard BuusQueen Mary University of London, Barts and The London School of Medicine and Dentistry, Blizard Institute, Centre for Cell Biology and Cutaneous Research, London, UK.
Manuela IezziAging Research Centre (Ce.S.I.), Foundation University "G. d'Annunzio", Chieti, Italy.
Francesca RicciLaboratory of Molecular Pharmacology IRCCS-Istituto di Ricerche Farmacologiche "Mario Negri", Milan, Italy.
Daniele BergamaschiQueen Mary University of London, Barts and The London School of Medicine and Dentistry, Blizard Institute, Centre for Cell Biology and Cutaneous Research, London, UK.
Paola OstanoCancer Genomics Laboratory, Fondazione Edo and Elvo Tempia, Biella, Italy.
Giovanna ChiorinoCancer Genomics Laboratory, Fondazione Edo and Elvo Tempia, Biella, Italy.
Rossano LattanzioAging Research Centre (Ce.S.I.), Foundation University "G. d'Annunzio", Chieti, Italy.
Massimo BrogginiLaboratory of Molecular Pharmacology IRCCS-Istituto di Ricerche Farmacologiche "Mario Negri", Milan, Italy.
Mauro PiantelliAging Research Centre (Ce.S.I.), Foundation University "G. d'Annunzio", Chieti, Italy.
Tania MaffucciQueen Mary University of London, Barts and The London School of Medicine and Dentistry, Blizard Institute, Centre for Cell Biology and Cutaneous Research, London, UK.
Marco FalascaQueen Mary University of London, Barts and The London School of Medicine and Dentistry, Blizard Institute, Centre for Cell Biology and Cutaneous Research, London, UK.
Queen Mary University of London · GBUniversity of Chieti-Pescara · ITFondazione Edo ed Elvo Tempia · ITMario Negri Institute for Pharmacological Research · ITCurtin University · AU

Funding

Prostate Cancer UK PG12-23Prostate Cancer UK PG13-029
6 · The paper itself

Abstract

It is now well established that the enzymes phosphoinositide 3-kinases (PI3Ks) have a key role in the development and progression of many cancer types and indeed PI3Ks inhibitors are currently being tested in clinical trials. Although eight distinct PI3K isoforms exist, grouped into three classes, most of the evidence currently available are focused on one specific isoform with very little known about the potential role of the other members of this family in cancer. Here we demonstrate that the class II enzyme PI3K-C2β is overexpressed in several human breast cancer cell lines and in human breast cancer specimens. Our data indicate that PI3K-C2β regulates breast cancer cell growth in vitro and in vivo and that PI3K-C2β expression in breast tissues is correlated with the proliferative status of the tumor. Specifically we show that downregulation of PI3K-C2β in breast cancer cell lines reduces colony formation, induces cell cycle arrest and inhibits tumor growth, in particular in an estrogen-dependent in vivo xenograft. Investigation of the mechanism of the PI3K-C2β-dependent regulation of cell cycle progression and cell growth revealed that PI3K-C2β regulates cyclin B1 protein levels through modulation of microRNA miR-449a levels. Our data further demonstrate that downregulation of PI3K-C2β inhibits breast cancer cell invasion in vitro and breast cancer metastasis in vivo. Consistent with this, PI3K-C2β is highly expressed in lymph-nodes metastases compared to matching primary tumors. These data demonstrate that PI3K-C2β plays a pivotal role in breast cancer progression and in metastasis development. Our data indicate that PI3K-C2β may represent a key molecular switch that regulates a rate-limiting step in breast tumor progression and therefore it may be targeted to limit breast cancer spread.

Indexed as

AnimalsBreast NeoplasmsCell Line, TumorCell ProliferationClass II Phosphatidylinositol 3-KinasesDisease ProgressionFemaleHeterograftsHumansMCF-7 CellsMiceMice, NudeSignal TransductionClass II Phosphatidylinositol 3-KinasesPIK3C2B protein, humanbreast cancercyclinB1metastasismiR449phosphoinositide 3-kinase C2β

Identifiers

PMID26934321
PMCPMC4951291
OpenAlexW2332552432

What OpenQuestion holds

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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.