Evidence map›Paper›PMID 23991171›Full record

ArticlePloS one2013

Loss of ZBRK1 contributes to the increase of KAP1 and promotes KAP1-mediated metastasis and invasion in cervical cancer.

Li-Fang Lin, Chien-Feng Li, Wei-Jan Wang, Wen-Ming Yang, Dennis Ding-Hwa Wang, Wen-Chang Chang, Wen-Hwa Lee, Ju-Ming Wang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.0field-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

29 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Multifaceted role ofMedComm · 2024
    Review
  3. KAP1 stabilizes MYCN mRNA and promotes neuroblastoma tumorigenicity by protecting the RNA mJournal of experimental & clinical cancer research : CR · 2024
    Article
  4. TRIM28 in cancer and cancer therapy.Frontiers in genetics · 2024
    Review
  5. Article
  6. Article
  7. Review
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  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Oncotarget · 2018
    Article
  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

8 authors at 4 institutions in 1 country.

Li-Fang LinInstitute of Basic Medical Sciences, National Cheng Kung University, Tainan City, Taiwan, Republic of China.
Chien-Feng Li
Wei-Jan Wang
Wen-Ming Yang
Dennis Ding-Hwa Wang
Wen-Chang Chang
Wen-Hwa Lee
Ju-Ming Wang
National Cheng Kung University · TWTaipei Medical University · TWChi Mei Medical Center · TWNational Chung Hsing University · TW

Funding

Translational Research in Cancer Genomic MedicineT32CA113265 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI LEE, WEN-HWA · 2007 to 2011
$1.4M
BLRD VA IK2 BX006111NCI NIH HHS T32 CA113265
6 · The paper itself

Abstract

ZBRK1, a zinc finger protein that interacts with breast cancer 1 (BRCA1) and KRAB-ZFP-associated protein 1 (KAP1), has been suggested to serve as a tumor suppressor via repression of tumor metastasis/invasion. To date, the detailed molecular mechanisms for how BRCA1 and KAP1 participate in ZBRK1-mediated transcriptional repression, metastasis and invasion as well as the associated clinical relevance remain unclear. In this study, we demonstrated that both the N- and C-terminal domains of ZBRK1 are important for inhibiting cell proliferation and anchorage-independent growth in cervical cancer. Specifically, the N-terminal KRAB domain of ZBRK1 displayed a more crucial role in inhibiting metastasis and invasion through modulation of KAP1 function in a transcriptionally dependent manner. The loss of ZBRK1 results in an increase of KAP1 expression, which enhanced migration and invasion of cervical cancer cells both the in vitro and in vivo. Moreover, an inverse correlation of expression levels was observed between ZBRK1 and KAP1 following tumor progression from in situ carcinoma to invasive/metastatic cervical cancer specimens. Taken together, the current results indicate that a loss of ZBRK1 contributes to the increased expression of KAP1, potentiating its role to enhance metastasis and invasion.

Indexed as

Neoplasm InvasivenessNeoplasm MetastasisBRCA1 ProteinCell ProliferationFemaleHeLa CellsHumansPromoter Regions, GeneticProtein BindingRepressor ProteinsTripartite Motif-Containing Protein 28Uterine Cervical NeoplasmsBRCA1 ProteinBRCA1 protein, humanRepressor ProteinsTRIM28 protein, humanTripartite Motif-Containing Protein 28ZNF350 protein, human

Identifiers

PMID23991171
PMCPMC3749996
OpenAlexW2038841550

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.