Evidence map›Paper›PMID 29980791›Full record

ArticleOncogene2018

ARID1A and CEBPα cooperatively inhibit UCA1 transcription in breast cancer.

Xiao Guo, Yin Zhang, Anand Mayakonda, Vikas Madan, Ling-Wen Ding, Le-Hang Lin, Saadiya Zia, Sigal Gery, Jeffrey W Tyner, Wu Zhou and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2018. 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
1.6field-weighted citation impact, top 16% 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, 34 citations in OpenAlex.

  1. Article
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  7. Article
  8. TGF-β1/Smad3 upregulates UCA1 to promote liver fibrosis through DKK1 and miR18a.Journal of molecular medicine (Berlin, Germany) · 2022
    Article
  9. Article
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  12. Article
  13. Review
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  15. Article
  16. Long non-coding RNAs: the tentacles of chromatin remodeler complexes.Cellular and molecular life sciences : CMLS · 2021
    Review
  17. Review
  18. Article
  19. Article
  20. Review
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

13 authors at 5 institutions in 3 countries.

Xiao GuoGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Research Center of Medicine, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China. guoxiao152@163.com.
Yin ZhangGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Research Center of Medicine, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China.
Anand MayakondaCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Vikas MadanCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.ORCID http://orcid.org/0000-0001-7876-624X
Ling-Wen DingCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.ORCID http://orcid.org/0000-0003-0022-1551
Le-Hang LinGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Research Center of Medicine, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China.
Saadiya ZiaDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Sigal GeryDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Jeffrey W TynerDepartment of Cell, Developmental and Cancer Biology, Oregon Health and Science University, Portland, OR, USA.
Wu ZhouDepartment of Medicine, College of Medicine and Health, Lishui University, Zhejiang, China.
Dong YinGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Research Center of Medicine, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China.
De-Chen LinDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA. De-Chen.Lin@cshs.org.
H Phillip KoefflerDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Cedars-Sinai Medical Center · USNational University of Singapore · SGSun Yat-sen University · CNLishui University · CNOregon Health & Science University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As one of the primary members of SWI/SNF chromatin remodeling complexes, ARID1A contains frequent loss-of-function mutations in many types of cancers. However, the molecular mechanisms underlying ARID1A deficiency in cancer biology remain to be investigated. Using breast cancer as a model, we report that silencing ARID1A significantly increased cellular proliferation and migration. Mechanistically, primarily functioning as a transcriptional repressor, loss of ARID1A profoundly alters histone modifications and the transcriptome. Notably, ARID1A inhibited the expression of a long non-coding RNA, UCA1, by regulating chromatin access of the transcription factor CEBPα. Restoration experiments showed that UCA1 mediates the functions of ARID1A that induces loss of cellular proliferation and migration. Together, our findings characterize ARID1A as a key tumor-suppressor gene in breast cancer through cooperation with CEBPα, and loss-of-function mutations of ARID1A activates UCA1.

Indexed as

AnimalsBreast NeoplasmsCCAAT-Enhancer-Binding ProteinsCell Line, TumorDNA-Binding ProteinsFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesGenes, Tumor SuppressorHeterograftsHumansMiceMice, NudeNuclear ProteinsRNA, Long NoncodingTranscription FactorsARID1A protein, humanCCAAT-Enhancer-Binding ProteinsCEBPA protein, humanDNA-Binding ProteinsNuclear ProteinsRNA, Long NoncodingTranscription FactorsUCA1 RNA, human

Identifiers

PMID29980791
OpenAlexW2882599759

What OpenQuestion holds

Textmetadata
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.