Evidence map›Paper›PMID 21496299›Full record

ArticleReproductive biology and endocrinology : RB&E2011

Depletion of the histone chaperone tNASP inhibits proliferation and induces apoptosis in prostate cancer PC-3 cells.

Oleg M Alekseev, Richard T Richardson, James K Tsuruta, Michael G O'Rand

Open access · goldAbstract readEvaluation Study
In one paragraph

Article in Reproductive biology and endocrinology : RB&E, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Nuclear Autoantigenic Sperm Protein Promotes Cardiac Regeneration and Repair Through Activating the PDGFRB/AKT Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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  15. Downregulation of tNASP inhibits proliferation through regulating cell cycle-related proteins and inactive ERK/MAPK signal pathway in renal cell carcinoma cells.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

4 authors at 1 institution in 1 country.

Oleg M AlekseevDepartment of Cell and Developmental Biology, University of North Carolina, Chapel Hill, NC 27599, USA. oleg_alekseev@med.unc.edu
Richard T Richardson
James K Tsuruta
Michael G O'Rand
University of North Carolina at Chapel Hill · US

Funding

TESTIS SPECIFIC HISTONE BINDING PROTEIN (NASP)U54HD035041 · NICHD · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PETRUSZ, PETER · 1997 to 2011
$16.1M
NICHD NIH HHS U54 (HD35041)
6 · The paper itself

Abstract

backgroundNASP (Nuclear Autoantigenic Sperm Protein) is a histone chaperone that is present in all dividing cells. NASP has two splice variants: tNASP and sNASP. Only cancer, germ, transformed, and embryonic cells have a high level of expression of the tNASP splice variant. We examined the consequences of tNASP depletion for prostate cancer PC-3 cells.

methodstNASP was depleted from prostate cancer PC-3 cells, cervical cancer HeLa cells, and prostate epithelial PWR-1E cells using lentivirus expression of tNASP shRNA. Cell cycle changes were studied by proliferation assay with CFSE labeling and double thymidine synchronization. Gene expression profiles were detected using RT(2)Profiler PCR Array, Western and Northern blotting.

resultsPC-3 and HeLa cells showed inhibited proliferation, increased levels of cyclin-dependant kinase inhibitor p21 protein and apoptosis, whereas non-tumorigenic PWR-1E cells did not. All three cell types showed decreased levels of HSPA2. Supporting in vitro experiments demonstrated that tNASP, but not sNASP is required for activation of HSPA2.

conclusionsOur results demonstrate that PC-3 and HeLa cancer cells require tNASP to maintain high levels of HSPA2 activity and therefore viability, while PWR-1E cells are unaffected by tNASP depletion. These different cellular responses most likely arise from changes in the interaction between tNASP and HSPA2 and disturbed tNASP chaperoning of linker histones. This study has demonstrated that tNASP is critical for the survival of prostate cancer cells and suggests that targeting tNASP expression can lead to a new approach for prostate cancer treatment.

Indexed as

AdenocarcinomaApoptosisAutoantigensCell CycleCell Line, TumorCell ProliferationDown-RegulationGene Knockdown TechniquesHeLa CellsHistone ChaperonesHumansMaleNuclear ProteinsProstatic NeoplasmsRNA, Small InterferingAutoantigensHistone ChaperonesNASP protein, humanNuclear ProteinsRNA, Small Interfering

Identifiers

PMID21496299
PMCPMC3100250
OpenAlexW2127418796

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.