Evidence map›Paper›PMID 11313980›Full record

ArticleOncogene2001

Mechanisms of regulation of cell adhesion and motility by insulin receptor substrate-1 in prostate cancer cells.

K Reiss, J Y Wang, G Romano, X Tu, F Peruzzi, R Baserga

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Nuclear IRS-1 and cancer.Journal of cellular physiology · 2012
    Review
  7. Article
  8. Article
  9. IGF-IR in neuroprotection and brain tumors.Frontiers in bioscience (Landmark edition) · 2009
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

6 authors at 3 institutions in 1 country.

K ReissKimmel Cancer Center, Thomas Jefferson University, 624 Biology Life Science Building, 233 South 10th Street, Philadelphia, Pennsylvania, PA 19107, USA.
J Y Wang
G Romano
X Tu
F Peruzzi
R Baserga
Thomas Jefferson University · USSidney Kimmel Cancer Center · USTemple University · US

Funding

VIRAL MODEL FOR TUMOR PATHOGENESIS IN BRAINP01NS036466 · NINDS · TEMPLE UNIV OF THE COMMONWEALTH · PI REISS, KRZYSZTOF · 1996 to 2007
$6.6M
REGULATION OF CELL PROLIFERATION BY GENES OF THE MYB FAMILYP01CA056309 · NCI · THOMAS JEFFERSON UNIVERSITY · PI GIORDANO, ANTONIO · 1991 to 2001
$1.4M
THE IGFI RECEPTOR IN AGINGR01AG016291 · NIA · THOMAS JEFFERSON UNIVERSITY · PI BASERGA, RENATO LUIGI · 1999 to 2003
$1.1M
NCI NIH HHS CA 56309NIA NIH HHS AG 16291NINDS NIH HHS P0-1 NS 36466
6 · The paper itself

Abstract

LNCaP cells are human prostatic cancer cells that have a frame-shift mutation of the tumor suppressor gene PTEN and do not express the insulin receptor substrate-1 (IRS-1), a major substrate of the type 1 insulin-like growth factor receptor (IGF-IR). Ectopic expression of IRS-1 in LNCaP cells increases cell adhesion and decreases cell motility by an IGF-I-independent mechanism. We show now that these effects of IRS-1 are accompanied by serine phosphorylation of IRS-1 and are inhibited by inhibitors of phosphatidylinositol 3-kinase (PI3K). We have confirmed the requirement for PI3K activity and serine phosphorylation by the use of IRS-1 mutants, expressed in LNCaP cells. Serine phosphorylation inhibits IGF-I-induced tyrosyl phosphorylation of IRS-1, which is restored by the expression of wild-type PTEN or by inhibition of PI3K activity. Finally, IRS-1 in LNCaP cells co-immunoprecipitates with integrin alpha 5 beta 1, and the association is again IGF-I-independent. We conclude that in LNCaP cells, IRS-1 is serine phosphorylated by PI3K, generating effects that are different, and even opposite, from those generated by IGF-I.

Indexed as

Cell AdhesionCell MovementAdenocarcinomaCollagenFibronectinsHumansInsulin Receptor Substrate ProteinsMaleMutationPhosphoinositide-3 Kinase InhibitorsPhosphoproteinsPhosphorylationProstatic NeoplasmsProtein BindingReceptors, FibronectinCollagenFibronectinsInsulin Receptor Substrate ProteinsIRS1 protein, humanPhosphoinositide-3 Kinase InhibitorsPhosphoproteinsReceptors, Fibronectin

Identifiers

PMID11313980
OpenAlexW2068602250

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.