Evidence map›Paper›PMID 25834103›Full record

ArticleOncotarget2015

Lipin-1 regulates cancer cell phenotype and is a potential target to potentiate rapamycin treatment.

Laura Brohée, Stéphane Demine, Jérome Willems, Thierry Arnould, Alain C Colige, Christophe F Deroanne

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 77 citations in OpenAlex.

  1. Review
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  3. Article
  4. Review
  5. Introduction ofIranian journal of basic medical sciences · 2024
    Article
  6. Review
  7. Evaluation ofAdvanced biomedical research · 2024
    Article
  8. Role of lipins in cardiovascular diseases.Lipids in health and disease · 2023
    Review
  9. Article
  10. Article
  11. Targeting the βThe Journal of pathology · 2023
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Ribosomal Protein S6: A Potential Therapeutic Target against Cancer?International journal of molecular sciences · 2021
    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

6 authors at 2 institutions in 1 country.

Laura BrohéeLaboratory of Connective Tissues Biology, GIGA-Cancer, University of Liège, Tour de Pathologie, Sart-Tilman, Belgium.
Stéphane DemineLaboratory of Biochemistry and Cell Biology (URBC), NARILIS (Namur Research Institute for Life Sciences), University of Namur (UNamur), Namur, Belgium.
Jérome WillemsLaboratory of Connective Tissues Biology, GIGA-Cancer, University of Liège, Tour de Pathologie, Sart-Tilman, Belgium.
Thierry ArnouldLaboratory of Biochemistry and Cell Biology (URBC), NARILIS (Namur Research Institute for Life Sciences), University of Namur (UNamur), Namur, Belgium.
Alain C ColigeLaboratory of Connective Tissues Biology, GIGA-Cancer, University of Liège, Tour de Pathologie, Sart-Tilman, Belgium.
Christophe F DeroanneLaboratory of Connective Tissues Biology, GIGA-Cancer, University of Liège, Tour de Pathologie, Sart-Tilman, Belgium.
University of Liège · BEUniversity of Namur · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipogenesis inhibition was reported to induce apoptosis and repress proliferation of cancer cells while barely affecting normal cells. Lipins exhibit dual function as enzymes catalyzing the dephosphorylation of phosphatidic acid to diacylglycerol and as co-transcriptional regulators. Thus, they are able to regulate lipid homeostasis at several nodal points. Here, we show that lipin-1 is up-regulated in several cancer cell lines and overexpressed in 50 % of high grade prostate cancers. The proliferation of prostate and breast cancer cells, but not of non-tumorigenic cells, was repressed upon lipin-1 knock-down. Lipin-1 depletion also decreased cancer cell migration through RhoA activation. Lipin-1 silencing did not significantly affect global lipid synthesis but enhanced the cellular concentration of phosphatidic acid. In parallel, autophagy was induced while AKT and ribosomal protein S6 phosphorylation were repressed. We also observed a compensatory regulation between lipin-1 and lipin-2 and demonstrated that their co-silencing aggravates the phenotype induced by lipin-1 silencing alone. Most interestingly, lipin-1 depletion or lipins inhibition with propranolol sensitized cancer cells to rapamycin. These data indicate that lipin-1 controls main cellular processes involved in cancer progression and that its targeting, alone or in combination with other treatments, could open new avenues in anticancer therapy.

Indexed as

LipogenesisAntibiotics, AntineoplasticAntineoplastic Combined Chemotherapy ProtocolsApoptosisAutophagyBreast NeoplasmsCell Line, TumorCell MovementCell ProliferationCell SurvivalDose-Response Relationship, DrugFemaleHumansMaleMolecular Targeted TherapyNuclear ProteinsAntibiotics, AntineoplasticLPIN1 protein, humanLPIN2 protein, humanMTOR protein, humanNuclear ProteinsPhosphatidate PhosphatasePropranololProto-Oncogene Proteins c-aktrhoA GTP-Binding ProteinRHOA protein, humanRibosomal Protein S6SirolimusTOR Serine-Threonine Kinaseslipin-1metabolismprostate cancerrapamycinRhoA

Identifiers

PMID25834103
PMCPMC4484455
OpenAlexW1501141911

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.