Evidence map›Paper›PMID 16966377›Full record

ArticleMolecular and cellular biology2006

The HBP1 transcriptional repressor participates in RAS-induced premature senescence.

Xiaowei Zhang, Jiyoung Kim, Robin Ruthazer, Michael A McDevitt, David E Wazer, K Eric Paulson, Amy S Yee

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

38 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
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  5. Review
  6. HBP1-mediated transcriptional repression of AFP inhibits hepatoma progression.Journal of experimental & clinical cancer research : CR · 2021
    Article
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  19. HMGB1 in health and disease.Molecular aspects of medicine · 2014
    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

7 authors at 3 institutions in 1 country.

Xiaowei ZhangDepartment of Biochemistry, Tufts University School of Medicine, Boston, MA 02111, USA.
Jiyoung Kim
Robin Ruthazer
Michael A McDevitt
David E Wazer
K Eric Paulson
Amy S Yee
Tufts Medical Center · USTufts University · USJohns Hopkins Medicine · US

Funding

PILOT AND FEASIBILITY STUDIESP30DK034928 · NIDDK · TUFTS MEDICAL CENTER · PI PLAUT, ANDREW GEORGE · 1986 to 2007
$8.5M
Phytonutrient Suppression of Wnt Signalling in CancerR01CA104236 · NCI · TUFTS UNIVERSITY BOSTON · PI YEE, AMY S. · 2005 to 2009
$1.6M
Mechanisms of Transcriptional Repressor HBP1 in CancerR01CA094187 · NCI · TUFTS UNIVERSITY BOSTON · PI YEE, AMY S. · 2002 to 2006
$1.4M
NCI NIH HHS CA-104236NCI NIH HHS CA-94187NCI NIH HHS R01 CA094187NCI NIH HHS R01 CA104236NIDDK NIH HHS DK34928NIDDK NIH HHS P30 DK034928
6 · The paper itself

Abstract

Oncogene-mediated premature senescence has emerged as a potential tumor-suppressive mechanism in early cancer transitions. Previous work shows that RAS and p38 MAPK participate in premature senescence, but transcriptional effectors have not been identified. Here, we demonstrate that the HBP1 transcriptional repressor participates in RAS- and p38 MAPK-induced premature senescence. In cell lines, we had previously isolated HBP1 as a retinoblastoma (RB) target but have determined that it functions as a proliferation regulator by inhibiting oncogenic pathways as a transcriptional repressor. In primary cells, the results indicate that HBP1 is a necessary component of premature senescence by RAS and p38 MAPK. Similarly, a knockdown of WIP1 (a p38 MAPK phosphatase) induced premature senescence that also required HBP1. Furthermore, HBP1 requires regulation by RB, in which few transcriptional regulators for premature senescence have been shown. Together, the data suggest a model in which RAS and p38 MAPK signaling engage HBP1 and RB to trigger premature senescence. As an initial step toward clinical relevance, a bioinformatics approach shows that the relative expression levels of HBP1 and WIP1 correlated with decreased relapse-free survival in breast cancer patients. Together, these studies highlight p38 MAPK, HBP1, and RB as important components for a premature-senescence pathway with possible clinical relevance to breast cancer.

Indexed as

Cellular SenescenceBinding SitesBreast NeoplasmsCell LineDatabases, GeneticDNA ReplicationHigh Mobility Group ProteinsHumansModels, BiologicalOncogene Protein p21(ras)p38 Mitogen-Activated Protein KinasesPhosphoprotein PhosphatasesProtein Phosphatase 2CRepressor ProteinsRetinoblastoma ProteinSignal TransductionHBP1 protein, humanHigh Mobility Group ProteinsOncogene Protein p21(ras)p38 Mitogen-Activated Protein KinasesPhosphoprotein PhosphatasesPPM1D protein, humanProtein Phosphatase 2CRepressor ProteinsRetinoblastoma Protein

Identifiers

PMID16966377
PMCPMC1636767
OpenAlexW2159782036

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.