Evidence map›Paper›PMID 27248326›Full record

ArticleOncotarget2016

Xist reduction in breast cancer upregulates AKT phosphorylation via HDAC3-mediated repression of PHLPP1 expression.

Yen-Sung Huang, Che-Chang Chang, Szu-Shuo Lee, Yuh-Shan Jou, Hsiu-Ming Shih

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
9.9field-weighted citation impact, top 1% 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

66 citing papers in PubMed, 103 citations in OpenAlex.

  1. Review
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  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Potential roles of lncRNA-XIST/miRNAs/mRNAs in human cancer cells.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
  12. Review
  13. Article
  14. Article
  15. Long noncoding RNAGenes & diseases · 2022
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

6 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 1 country.

Yen-Sung HuangInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Che-Chang ChangGraduate Institute of Translational Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
Szu-Shuo LeeProgram in Molecular Medicine, National Yang-Ming University and Academia Sinica, Taipei, Taiwan.
Yuh-Shan JouInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Hsiu-Ming ShihInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
National Yang Ming Chiao Tung University · TWTaipei Medical University · TWInstitute of Biomedical Sciences, Academia Sinica · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long noncoding RNAs (lncRNAs) dysregulated in cancer potentially play oncogenic or tumor-suppressive roles. While the X inactivate-specific transcript (Xist) lncRNA is important for X-chromosome inactivation in female cells, very little is known about the role of Xist in human breast cancer in modulating cellular pathway(s). Here, we show that Xist expression is significantly reduced in breast tumor samples and cancer cell lines. Xist knockdown or overexpression resulted in increased or decreased levels, respectively, of AKT phosphorylation and cell viability. Further studies revealed an inverse correlation between Xist and phospho-AKT levels in breast cancer samples. Additionally, Xist knockdown-elicited increase of cell viability was attenuated by AKT inhibitor. These results suggest that Xist negatively regulates cell viability via inhibition of AKT activation. Interestingly, decreased Xist expression in breast cancer samples was associated with reduced levels of Jpx RNA, an lncRNA that positively regulates Xist promoter activity. Accordingly, Jpx knockdown enhanced AKT activation and cell viability. We also demonstrate that knockdown of Xist or SPEN, an intermediator protein to link Xist, SMRT co-repressor and HDAC3 complexes for X-chromosome inactivation, decreased expression of PHLPP1, a phosphatase to remove AKT phosphorylation, via increased HDAC3 recruitment to the PHLPP1 promoter, correlating with increased AKT phosphorylation. Our findings elucidate the tumor suppressor role of Xist in breast cancer and provide the molecular basis of Xist in downregulating AKT activation.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsBreast NeoplasmsCell SurvivalDatasets as TopicDNA-Binding ProteinsDown-RegulationFemaleGene Knockdown TechniquesGenes, Tumor SuppressorHistone Deacetylase 3Histone DeacetylasesHomeodomain ProteinsHumansMCF-7 CellsMiceDNA-Binding ProteinsHistone Deacetylase 3Histone DeacetylasesHomeodomain ProteinsNCOR2 protein, humanNuclear ProteinsNuclear Receptor Co-Repressor 2PHLPP1 protein, humanPhosphoprotein PhosphatasesProto-Oncogene Proteins c-aktRNA-Binding ProteinsRNA, Long NoncodingRNA, Small InterferingSPEN protein, humanXIST non-coding RNAAKTbreast cancerHDAC3lncRNAXist

Identifiers

PMID27248326
PMCPMC5190021
OpenAlexW2406645435

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.