Evidence map›Paper›PMID 22870275›Full record

ArticlePloS one2012

Crucial role of TSC-22 in preventing the proteasomal degradation of p53 in cervical cancer.

Cheol-Hee Yoon, Seung Bae Rho, Seong-Tae Kim, Seongho Kho, Junsoo Park, Ik-Soon Jang, Seonock Woo, Sung Soon Kim, Je-Ho Lee, Seung-Hoon Lee

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
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  7. Molecular Patho-mechanisms of cervical cancer (MMP1).Annals of medicine and surgery (2012) · 2022
    Review
  8. Article
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  13. Yeast two-hybrid screening identified WDR77 as a novel interacting partner of TSC22D2.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  14. Article
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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

10 authors at 7 institutions in 1 country.

Cheol-Hee YoonDivision of AIDS, Center for Immunology and Pathology, National Institute of Health, Cheongwon-gun, Chungbuk, Korea.
Seung Bae Rho
Seong-Tae Kim
Seongho Kho
Junsoo Park
Ik-Soon Jang
Seonock Woo
Sung Soon Kim
Je-Ho Lee
Seung-Hoon Lee
Korea National Institute of Health · KRYong In University · KRKorea Basic Science Institute · KRKorea Institute of Ocean Science and Technology · KRNational Cancer Center · KRSamsung Medical Center · KRYonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The p53 tumor suppressor function can be compromised in many tumors by the cellular antagonist HDM2 and human papillomavirus oncogene E6 that induce p53 degradation. Restoration of p53 activity has strong therapeutic potential. Here, we identified TSC-22 as a novel p53-interacting protein and show its novel function as a positive regulator of p53. We found that TSC-22 level was significantly down-regulated in cervical cancer tissues. Moreover, over-expression of TSC-22 was sufficient to inhibit cell proliferation, promote cellular apoptosis in cervical cancer cells and suppress growth of xenograft tumors in mice. Expression of also TSC-22 enhanced the protein level of p53 by protecting it from poly-ubiquitination. When bound to the motif between amino acids 100 and 200 of p53, TSC-22 inhibited the HDM2- and E6-mediated p53 poly-ubiquitination and degradation. Consequently, ectopic over-expression of TSC-22 activated the function of p53, followed by increased expression of p21(Waf1/Cip1) and PUMA in human cervical cancer cell lines. Interestingly, TSC-22 did not affect the interaction between p53 and HDM2. Knock-down of TSC-22 by small interfering RNA clearly enhanced the poly-ubiquitination of p53, leading to the degradation of p53. These results suggest that TSC-22 acts as a tumor suppressor by safeguarding p53 from poly-ubiquitination mediated-degradation.

Indexed as

ProteolysisUbiquitinationAnimalsApoptosisCell ProliferationDown-RegulationFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHeLa CellsHumansMiceMice, Inbred BALB CMice, NudeProteasome Endopeptidase ComplexProto-Oncogene Proteins c-mdm2MDM2 protein, humanProteasome Endopeptidase ComplexProto-Oncogene Proteins c-mdm2Repressor ProteinsRNA, Small InterferingTP53 protein, humanTSC22D1 protein, humanTumor Suppressor Protein p53

Identifiers

PMID22870275
PMCPMC3411576
OpenAlexW2071247399

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.