Evidence map›Paper›PMID 20962042›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2010

Prolactin inhibits activity of pyruvate kinase M2 to stimulate cell proliferation.

Bentley Varghese, Gayathri Swaminathan, Alexander Plotnikov, Christos Tzimas, Ning Yang, Hallgeir Rui, Serge Y Fuchs

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

11 citing papers in PubMed, 25 citations in OpenAlex.

  1. The PI3K/Akt Pathway and Glucose Metabolism: A Dangerous Liaison in Cancer.International journal of biological sciences · 2024
    Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. A critical review of the role of MBiochimica et biophysica acta. Reviews on cancer · 2019
    Review
  8. Article
  9. Pyruvate kinase: Function, regulation and role in cancer.Seminars in cell & developmental biology · 2015
    Review
  10. Article
  11. PKM2, a Central Point of Regulation in Cancer Metabolism.International journal of cell biology · 2013
    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 3 institutions in 1 country.

Bentley VargheseDepartment of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104-4539, USA.
Gayathri Swaminathan
Alexander Plotnikov
Christos Tzimas
Ning Yang
Hallgeir Rui
Serge Y Fuchs
University of Pennsylvania · USSidney Kimmel Cancer Center · USThomas Jefferson University · US

Funding

IMMUNOBIOLOGY OF NORMAL AND NEOPLASTIC LYMPHOCYTEST32CA009140 · NCI · UNIVERSITY OF PENNSYLVANIA · PI Malay Haldar, WARREN S PEAR · 1985 to 2026
$16.1M
Experimental Modeling of Human Breast Cancer in MiceR01CA118740 · NCI · THOMAS JEFFERSON UNIVERSITY · PI RUI, HALLGEIR · 2008 to 2012
$1.8M
Stability of prolactin receptor and prolactin signalingR01CA115281 · NCI · UNIVERSITY OF PENNSYLVANIA · PI FUCHS, SERGE Y · 2006 to 2010
$1.4M
NCI NIH HHS CA115281NCI NIH HHS CA118740NCI NIH HHS R01 CA115281NCI NIH HHS R01 CA118740NCI NIH HHS T32 CA009140NCI NIH HHS T32CA09140
6 · The paper itself

Abstract

Mitogenic and prosurvival effects underlie the tumorigenic roles of prolactin (PRL) in the pathogenesis of breast cancer. PRL signaling is mediated through its receptor (PRLr). A proteomics screen identified the pyruvate kinase M2 (PKM2), a glycolytic enzyme known to play an important role in tumorigenesis, as a protein that constitutively interacts with PRLr. Treatment of cells with PRL inhibited pyruvate kinase activity and increased the lactate content in human cells in a manner that was dependent on the abundance of PRLr, activation of Janus kinase 2, and tyrosine phosphorylation of the intracellular domain of PRLr. Knockdown of PKM2 attenuated PRL-stimulated cell proliferation. The extent of this proliferation was rescued by the knock-in of the wild-type PKM2 but not of its mutant insensitive to PRL-mediated inhibition. We discuss a hypothesis that the inhibition of PKM2 by PRL contributes to the PRL-stimulated cell proliferation.

Indexed as

AnimalsBreast NeoplasmsCell Growth ProcessesCell LineCell Line, TumorGene Knockdown TechniquesGene Knock-In TechniquesHumansJanus Kinase 2Lactic AcidPhosphorylationProlactinPyruvate KinaseRatsReceptors, ProlactinSignal TransductionJAK2 protein, humanJanus Kinase 2Lactic AcidProlactinPyruvate KinaseReceptors, ProlactinTyrosine

Identifiers

PMID20962042
PMCPMC2999476
OpenAlexW1992885167

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.