Evidence map›Paper›PMID 23208500›Full record

ArticleOncogene2013

Induction of p53, p21 and apoptosis by silencing the NF90/NF45 complex in human papilloma virus-transformed cervical carcinoma cells.

R A Shamanna, M Hoque, T Pe'ery, M B Mathews

Abstract read
In one paragraph

Article in Oncogene, 2013. 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
3.3field-weighted citation impact, top 8% 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, 63 citations in OpenAlex.

  1. Review
  2. Review
  3. The Polyvalent Role of NF90 in RNA Biology.International journal of molecular sciences · 2022
    Review
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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 2 institutions in 1 country.

R A Shamanna1] Department of Biochemistry and Molecular Biology, New Jersey Medical School, UMDNJ, Newark, NJ, USA [2] Graduate School of Biomedical Sciences, UMDNJ, Newark, NJ, USA.
M Hoque
T Pe'ery
M B Mathews
Rutgers, The State University of New Jersey · USRutgers New Jersey Medical School

Funding

Functions of Double-stranded RNA Binding ProteinsR01AI034552 · NIAID · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI MATHEWS, MICHAEL B · 1993 to 2008
$4.4M
NIAID NIH HHS R01 AI034552
6 · The paper itself

Abstract

The heterodimeric nuclear factor (NF) 90/NF45 complex (NF90/NF45) binds nucleic acids and is a multifunctional regulator of gene expression. Here we report that depletion of NF90/NF45 restores the expression of the p53 and p21 proteins in cervical carcinoma cells infected with high-risk human papillomaviruses (HPVs). Knockdown of either NF90 or NF45 by RNA interference led to greatly elevated levels of p53 and p21 proteins in HPV-derived HeLa and SiHa cells but not in other cancerous or normal cell lines. In HeLa cells, p21 messenger-RNA (mRNA) increased concomitantly but the level of p53 mRNA was unaffected. RNA interference directed against p53 prevented the induction of both proteins. These results indicated that the upregulation of p21 is due to p53-dependent transcription, whereas p53 is regulated post-transcriptionally. Proteasome-mediated turnover of p53 is accelerated by the HPV E6 and cellular E6AP proteins. We therefore examined the hypothesis that this pathway is regulated by NF90/NF45. Indeed, depletion of NF90 attenuated the expression of E6 RNA and inhibited transcription from the HPV early promoter, revealing a new role for NF90/NF45 in HPV gene expression. The transcription inhibition was largely independent of the reduction of P-TEFb (positive transcription elongation factor b) levels caused by NF90 depletion. Consistent with p53 derepression, NF90/NF45-depleted HeLa cells displayed elevated poly ADP-ribose polymerase (PARP) cleavage and susceptibility to camptothecin-induced apoptosis. We conclude that high-risk strains of HPV utilize the cellular NF90/NF45 complex for viral E6 expression in infected cervical carcinoma cell lines. Interference with NF90/NF45 function could assist in controlling cervical carcinoma.

Indexed as

ApoptosisCarcinomaCell Transformation, NeoplasticCyclin-Dependent Kinase Inhibitor p21DNA-Binding ProteinsFemaleGene Expression Regulation, NeoplasticHeLa CellsHuman papillomavirus 18HumansMultiprotein ComplexesNuclear Factor 45 ProteinNuclear Factor 90 ProteinsOncogene Proteins, ViralPapillomaviridaePoly (ADP-Ribose) Polymerase-1CDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21DNA-Binding ProteinsE6 protein, Human papillomavirus type 18ILF2 protein, humanILF3 protein, humanMultiprotein ComplexesNuclear Factor 45 ProteinNuclear Factor 90 ProteinsOncogene Proteins, ViralPARP1 protein, humanPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID23208500
PMCPMC4032571
OpenAlexW2034677367

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.