Evidence map›Paper›PMID 12368310›Full record

ArticleJournal of virology2002

Simian virus 40 small tumor antigen activates AKT and telomerase and induces anchorage-independent growth of human epithelial cells.

Hang Yuan, Tim Veldman, Kathleen Rundell, Richard Schlegel

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

36 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Oncology letters · 2018
    Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Inhibition of Cullin-RING E3 ubiquitin ligase 7 by simian virus 40 large T antigen.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  13. Article
  14. Article
  15. HijAkt: The PI3K/Akt pathway in virus replication and pathogenesis.Progress in molecular biology and translational science · 2012
    Review
  16. Review
  17. Article
  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

4 authors at 2 institutions in 1 country.

Hang YuanDepartment of Pathology, Georgetown University Medical School, Washington, DC 20007, USA.
Tim Veldman
Kathleen Rundell
Richard Schlegel
Georgetown University · USNorthwestern University · US

Funding

PAPILLOMAVIRUS E5 ONCOPROTEIN AND CELL TRANSFORMATIONR01CA053371 · NCI · GEORGETOWN UNIVERSITY · PI SCHLEGEL, RICHARD · 1991 to 2010
$5.0M
NCI NIH HHS R01 CA053371NCI NIH HHS R01CA53371
6 · The paper itself

Abstract

Human keratinocytes immortalized by full-length or early-region simian virus 40 (SV40) DNA grow in agarose and form tumors in nude mice, in contrast to keratinocytes immortalized by the E6/E7 genes of human papillomaviruses. To determine the molecular basis for this biological difference in growth, we have used the individual SV40 oncogenes (large T antigen [LT] and small t antigen [st]) and human papillomavirus oncogenes (E6/E7) to study the progression of human epithelial cells from the nonimmortal to the immortal state as well as from the immortal to the anchorage-independent state. Transfection of primary human foreskin keratinocytes with LT did not immortalize cells but did extend the in vitro life span and produced cells that were resistant to calcium- and serum-induced terminal differentiation. Cells transfected with st alone did not passage beyond vector-transfected keratinocytes. The simultaneous expression of LT- and st-immortalized keratinocytes occurred without evidence of crisis and, as anticipated, these immortal cells were anchorage- independent for growth. Interestingly, we found that keratinocytes expressing both LT and st, but not keratinocytes with LT alone, exhibited increased phosphorylation of the protein kinase AKT. In addition, AKT activation was paralleled by an increase in telomerase activity. Addition of st to anchorage-dependent keratinocytes, expressing either LT (nonimmortal) or E6/E7 (immortal), converted the cells to anchorage independence, with similar accompanying increases in AKT phosphorylation and telomerase activity. However, it was not possible to induce keratinocyte growth in agarose with activated AKT and/or overexpressed hTERT, indicating that these newly defined st-induced activities are not sufficient for progression to the anchorage-independent state.

Indexed as

Protein Serine-Threonine Kinases3T3 CellsAnimalsAntigens, Polyomavirus TransformingCell AdhesionCell DivisionCells, CulturedCell SurvivalDNA-Binding ProteinsEnzyme ActivationHumansKeratinocytesMicePhosphorylationProto-Oncogene ProteinsProto-Oncogene Proteins c-aktAKT1 protein, humanAntigens, Polyomavirus TransformingDNA-Binding ProteinsProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktTelomerase

Identifiers

PMID12368310
PMCPMC136600
OpenAlexW2110003347

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.