Evidence map›Paper›PMID 16055704›Full record

ArticleMolecular and cellular biology2005

PTEN represses RNA Polymerase I transcription by disrupting the SL1 complex.

Cheng Zhang, Lucio Comai, Deborah L Johnson

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

61 citing papers in PubMed, 100 citations in OpenAlex.

  1. Article
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  6. Article
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  8. Review
  9. Ribosome Biogenesis and Cancer: Overview on Ribosomal Proteins.International journal of molecular sciences · 2021
    Review
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  11. Article
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  18. Article
  19. Keeping ribosomal DNA intact: a repeating challenge.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2019
    Review
  20. Review

1 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Cheng ZhangDepartment of Biochemistry and Molecular Biology, University of Southern California, Keck School of Medicine, Los Angeles, 90033, USA.
Lucio Comai
Deborah L Johnson
University of Southern California · US

Funding

TATA-binding protein, a novel target of EGFR signalingR01CA074138 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JOHNSON, DEBORAH L. · 1997 to 2015
$3.6M
Novel targets that are deregulated by loss of PTENR01CA108614 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JOHNSON, DEBORAH L. · 2006 to 2016
$2.7M
NCI NIH HHS CA-074138NCI NIH HHS CA108614NCI NIH HHS R01 CA074138NCI NIH HHS R01 CA108614
6 · The paper itself

Abstract

PTEN is a tumor suppressor whose function is frequently lost in human cancer. It possesses a lipid phosphatase activity that represses the activation of PI3 kinase/Akt signaling, leading to decreased cell growth, proliferation, and survival. The potential for PTEN to regulate transcription of the large rRNAs by RNA polymerase I (RNA Pol I) was investigated. As increased synthesis of rRNAs is a hallmark of neoplastic transformation, the ability of PTEN to control the transcription of rRNAs might be crucial for its tumor suppressor function. The expression of PTEN in PTEN-deficient cells represses RNA Pol I transcription, while decreasing PTEN expression enhances transcription. PTEN-mediated repression requires its lipid phosphatase activity and is independent of the p53 status of the cell. This event can be uncoupled from PTEN's ability to regulate the cell cycle. RNA Pol I is regulated through PI3 kinase/Akt/mammalian target of rapamycin/S6 kinase, and the expression of constitutively activated S6 kinase is able to abrogate transcription repression by PTEN. No change in the expression of the RNA Pol I transcription components, upstream binding factor or SL1, was observed upon PTEN expression. However, chromatin immunoprecipitation assays demonstrate that PTEN differentially reduces the occupancy of the SL1 subunits on the rRNA gene promoter. Furthermore, PTEN induces dissociation of the SL1 subunits. Together, these results demonstrate that PTEN represses RNA Pol I transcription through a novel mechanism that involves disruption of the SL1 complex.

Indexed as

Transcription, GeneticCell Line, TumorChromatin ImmunoprecipitationCyclin D1DNADose-Response Relationship, DrugHumansImmunoblottingImmunoprecipitationPhosphatidylinositol 3-KinasesPhosphoric Monoester HydrolasesPol1 Transcription Initiation Complex ProteinsPromoter Regions, GeneticPTEN PhosphohydrolaseRibosomal Protein S6 KinasesRNA Polymerase ICyclin D1DNAPhosphatidylinositol 3-KinasesPhosphoric Monoester HydrolasesPol1 Transcription Initiation Complex ProteinsPTEN PhosphohydrolasePTEN protein, humanRibosomal Protein S6 KinasesRNA Polymerase IRNA, RibosomalRNA, Small InterferingSingle-Strand Specific DNA and RNA Endonucleasestranscription initiation factor TIF-IBTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID16055704
PMCPMC1190253
OpenAlexW2161972131

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.