Evidence map›Paper›PMID 21678403›Full record

ArticleJournal of cellular physiology2011

Hsp22 (HspB8/H11) knockdown induces Sam68 expression and stimulates proliferation of glioblastoma cells.

Suhasini Modem, Kannagi Chinnakannu, Uma Bai, G Prem-Veer Reddy, Thipparthi R Reddy

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular physiology, 2011. 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
1.2field-weighted citation impact, top 22% 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, 42 citations in OpenAlex.

  1. Review
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  13. Sam68 is Overexpressed in Epithelial Ovarian Cancer and Promotes Tumor Cell Proliferation.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Article
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  17. Sam68 promotes cellular proliferation and predicts poor prognosis in esophageal squamous cell carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  18. Clinical significance of Sam68 expression in endometrial carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
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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

5 authors at 2 institutions in 1 country.

Suhasini ModemDepartment of Immunology and Microbiology, Wayne State University, Detroit, Michigan 48201, USA.
Kannagi Chinnakannu
Uma Bai
G Prem-Veer Reddy
Thipparthi R Reddy
Henry Ford Hospital · USWayne State University · US

Funding

SAM68 AND HIV REPLICATIONR01AI046240 · NIAID · WAYNE STATE UNIVERSITY · PI REDDY, THIPPARTHI R · 2000 to 2002
$782k
Heat Shock Protein-22 and Rev Block In AstrocytesR03NS060650 · NINDS · WAYNE STATE UNIVERSITY · PI THIPPARTHI, RAGHAVENDAR R · 2007 to 2008
$151k
NIAID NIH HHS AI46240NIAID NIH HHS R01 AI046240NINDS NIH HHS NS060650NINDS NIH HHS R03 NS060650
6 · The paper itself

Abstract

Sam68 (Src-associated protein in mitosis 68 kDa) is a multifunctional protein, known to govern cellular signal transduction, transcription, RNA metabolism, proliferation, apoptosis, and HIV-1 replication. Although intrinsic mechanisms that modulate Sam68 function are beginning to emerge, the regulatory events contributing to its expression remain elusive. We previously reported that heat shock protein-22 (Hsp22) antagonizes Sam68 function in rev-response element (RRE)-mediated gene expression. We now demonstrate that Sam68 levels correlate inversely with Hsp22 in a variety of cells, including U87, Jurkat, 293T, and U-937. In U87 glioblastoma cells, which contained high levels of Hsp22 than other cell lines tested, Hsp22 knockdown dramatically increased both Sam68 mRNA and protein, altered cellular morphology, and enhanced cell proliferation. This heightened proliferation was associated with a sharp decrease in G(0) /G(1) and a corresponding increase in S and G(2) /M phases in exponentially growing cultures. The increased S phase population in turn correlated with enhanced expression of cell cycle regulatory proteins such as cyclin E, cyclin A, ribonucleotide reductase (RNR), and proliferating cell nuclear antigen (PCNA), which are required for the transition of cells from G(1) to S phase. Collectively, our results demonstrate for the first time that Hsp22 regulates Sam68 expression and the ratio of Sam68 to Hsp22 may determine the proliferative potential of glioblastoma cells.

Indexed as

Adaptor Proteins, Signal TransducingBrain NeoplasmsCell Cycle ProteinsCell Line, TumorCell ProliferationDNA-Binding ProteinsGene Expression Regulation, NeoplasticGene Knockdown TechniquesGlioblastomaHeat-Shock ProteinsHumansMolecular ChaperonesProtein Serine-Threonine KinasesRNA-Binding ProteinsAdaptor Proteins, Signal TransducingCell Cycle ProteinsDNA-Binding ProteinsHeat-Shock ProteinsHSPB8 protein, humanKHDRBS1 protein, humanMolecular ChaperonesProtein Serine-Threonine KinasesRNA-Binding Proteins

Identifiers

PMID21678403
PMCPMC3178715
OpenAlexW2117119973

What OpenQuestion holds

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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.