Evidence map›Paper›PMID 24276247›Full record

ArticleOncogene2014

Enhanced expression of transferrin receptor 1 contributes to oncogenic signalling by sphingosine kinase 1.

D H Pham, J A Powell, B L Gliddon, P A B Moretti, A Tsykin, M Van der Hoek, R Kenyon, G J Goodall, S M Pitson

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
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  3. Article
  4. Article
  5. METTL3-mediated mOncogene · 2021
    Article
  6. Frontiers in molecular biosciences · 2021
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Noncanonical role of transferrin receptor 1 is essential for intestinal homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  17. Article
  18. Article
  19. 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

9 authors at 4 institutions in 1 country.

D H Pham1] Centre for Cancer Biology, SA Pathology, Frome Road, Adelaide, SA, Australia [2] School of Molecular and Biomedical Science, University of Adelaide, Adelaide, SA, Australia.
J A PowellCentre for Cancer Biology, SA Pathology, Frome Road, Adelaide, SA, Australia.
B L GliddonCentre for Cancer Biology, SA Pathology, Frome Road, Adelaide, SA, Australia.
P A B MorettiCentre for Cancer Biology, SA Pathology, Frome Road, Adelaide, SA, Australia.
A Tsykin1] Centre for Cancer Biology, SA Pathology, Frome Road, Adelaide, SA, Australia [2] School of Molecular and Biomedical Science, University of Adelaide, Adelaide, SA, Australia.
M Van der HoekAdelaide Microarray Facility, SA Pathology, Frome Road, Adelaide, SA, Australia.
R KenyonAdelaide Microarray Facility, SA Pathology, Frome Road, Adelaide, SA, Australia.
G J Goodall1] Centre for Cancer Biology, SA Pathology, Frome Road, Adelaide, SA, Australia [2] School of Molecular and Biomedical Science, University of Adelaide, Adelaide, SA, Australia [3] School of Pharmacy and Medical Science, University of South Australia, Adelaide, SA, Australia.
S M Pitson1] Centre for Cancer Biology, SA Pathology, Frome Road, Adelaide, SA, Australia [2] School of Molecular and Biomedical Science, University of Adelaide, Adelaide, SA, Australia [3] School of Pharmacy and Medical Science, University of South Australia, Adelaide, SA, Australia.
Centre for Cancer Biology · AUSouth Australia Pathology · AUUniversity of Adelaide · AUUniversity of South Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sphingosine kinase 1 (SK1) is a lipid kinase that catalyses the formation of sphingosine-1-phosphate (S1P). Considerable evidence has implicated elevated cellular SK1 in tumour development, progression and disease severity. In particular, SK1 has been shown to enhance cell survival and proliferation and induce neoplastic transformation. Although S1P has been found to have both cell-surface G-protein-coupled receptors and intracellular targets, the specific downstream pathways mediating oncogenic signalling by SK1 remain poorly defined. Here, using a gene expression array approach, we have demonstrated a novel mechanism whereby SK1 regulates cell survival, proliferation and neoplastic transformation through enhancing expression of transferrin receptor 1 (TFR1). We showed that elevated levels of SK1 enhanced total as well as cell-surface TFR1 expression, resulting in increased transferrin uptake into cells. Notably, we also found that SK1 activation and localization to the plasma membrane, which are critical for its oncogenic effects, are necessary for regulation of TFR1 expression specifically through engagement of the S1P G-protein coupled receptor, S1P2. Furthermore, we showed that blocking TFR1 function with a neutralizing antibody inhibits SK1-induced cell proliferation, survival and neoplastic transformation of NIH3T3 fibroblasts. Similar effects were observed following antagonism of S1P2. Together these findings suggest that TFR1 has an important role in SK1-mediated oncogenesis.

Indexed as

AnimalsAntigens, CDCell LineCell Transformation, NeoplasticFluorescent Antibody TechniqueGene Expression RegulationGene Knockdown TechniquesHumansImmunoblottingMiceNeoplasmsOligonucleotide Array Sequence AnalysisPhosphotransferases (Alcohol Group Acceptor)Real-Time Polymerase Chain ReactionReceptors, TransferrinRNA, Small InterferingAntigens, CDCD71 antigenPhosphotransferases (Alcohol Group Acceptor)Receptors, TransferrinRNA, Small InterferingSphingosine Kinase

Identifiers

PMID24276247
OpenAlexW2024372331

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.