Evidence map›Paper›PMID 12149650›Full record

ArticleOncogene2002

PTEN, but not SHIP and SHIP2, suppresses the PI3K/Akt pathway and induces growth inhibition and apoptosis of myeloma cells.

Yong Choi, Jie Zhang, Cristina Murga, Hong Yu, Erich Koller, Brett P Monia, J Silvio Gutkind, Weiqun Li

Open access · bronzeAbstract readComparative Study
PubMed Publisher
In one paragraph

Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
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  17. Article
  18. Targeting the bone marrow in Waldenstrom macroglobulinemia.Clinical lymphoma, myeloma & leukemia · 2011
    Review
  19. Inhibitor and activator: dual functions for SHIP in immunity and cancer.Annals of the New York Academy of Sciences · 2011
    Review
  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

8 authors at 4 institutions in 1 country.

Yong ChoiLomabardi Cancer Center, Georgetown University Medical Center, Washington, District of Colombia 20007, USA.
Jie Zhang
Cristina Murga
Hong Yu
Erich Koller
Brett P Monia
J Silvio Gutkind
Weiqun Li
Georgetown University Medical Center · USIonis Pharmaceuticals (United States) · USNational Institute of Dental and Craniofacial Research · USGeorgetown University · US

Funding

Molecular Mechanisms Of Growth Control And CarcinogenesisZIADE000551 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI GUTKIND, JORGE SILVIO · 2009 to 2015
$11.5M
Oral CarcinogenesisZIADE000558 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI GUTKIND, JORGE SILVIO · 2009 to 2015
$11.4M
ORAL CARCINOGENESISZ01DE000558 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI GUTKIND, J · 1992 to 2008
$3.6M
ROLE OF G PROTEINS IN GROWTH CONTROL AND CARCINOGENESISZ01DE000551 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI GUTKIND, J · 1992 to 2008
$3.4M
6 · The paper itself

Abstract

Expression of PTEN tumor suppressor gene has been known to dephosphorylate the phosphatidylinositol 3' kinase (PI3K) products on the 3 prime inositol ring, resulting in reduced Akt activation. Loss of PTEN expression in OPM2 and delta47 human myeloma lines led to high Akt activity toward insulin-like growth factor I (IGF-I). In contrast, mouse plasma cell tumor (PCT) lines, expressing wild type PTEN, did not respond to IGF-I for Akt activation. We demonstrated here that endogenous PTEN played a negative role in controlling Akt activity in both mouse PCT and NIH3T3 fibroblast lines by using anti-sense oligonucleotides against PTEN. To determine the role of src-homology 2-containing inositol 5' phosphatase (SHIP) in regulating the PI3K/Akt pathway, we manipulated its expression by down-regulation and overexpression in myeloma, PCT and NIH3T3 lines and analysed Akt activation. Our results showed that SHIP, unlike PTEN, did not affect Akt activity in all systems analysed, despite its ability to dephosphorylate a PI3K product. Although SHIP2 expression resulted in suppression of interleukin-6-mediated mitogen-activated protein kinase activation, expression of SHIP and SHIP2 in a PTEN-null myeloma line did not suppress Akt activity. Biologically, expression of only PTEN, but not SHIP and SHIP2, resulted in growth inhibition and increased apoptosis in OPM2 myeloma line. Together, our results have established the role of PTEN, but not SHIP and SHIP2, in negatively regulating the PI3K/Akt cascade and in myeloma leukemogenesis.

Indexed as

ApoptosisProtein Serine-Threonine Kinases3T3 CellsAnimalsAnnexin A5Caspase 3CaspasesDown-RegulationFormazansGenes, Tumor SuppressorHistonesHumansImmunoblottingInsulin-Like Growth Factor IInterleukin-6MAP Kinase Signaling SystemAKT1 protein, humanAnnexin A5CASP3 protein, humanCasp3 protein, mouseCaspase 3CaspasesFormazansHistonesINPPL1 protein, humanInsulin-Like Growth Factor IInterleukin-6MTT formazanOligonucleotides, AntisensePhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPhosphatidylinositol 3-KinasesPhosphoric Monoester HydrolasesProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanTetrazolium SaltsTumor Suppressor Proteins

Identifiers

PMID12149650
OpenAlexW2066425902

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.