Evidence map›Paper›PMID 27028856›Full record

ArticleOncotarget2016

Sumoylation of TCF21 downregulates the transcriptional activity of estrogen receptor-alpha.

Xiang Ao, Shujing Li, Zhaowei Xu, Yangyang Yang, Min Chen, Xiao Jiang, Huijian Wu

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 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. The Role of SUMO E3 Ligases in Signaling Pathway of Cancer Cells.International journal of molecular sciences · 2022
    Review
  3. Article
  4. Review
  5. Role of the bHLH transcription factor TCF21 in development and tumorigenesis.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021
    Review
  6. TCF21: a critical transcription factor in health and cancer.Journal of molecular medicine (Berlin, Germany) · 2020
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. 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

7 authors at 2 institutions in 1 country.

Xiang AoSchool of Life Science and Biotechnology, Dalian University of Technology, Dalian 116024, Liaoning, People's Republic of China.
Shujing LiSchool of Life Science and Biotechnology, Dalian University of Technology, Dalian 116024, Liaoning, People's Republic of China.
Zhaowei XuSchool of Life Science and Biotechnology, Dalian University of Technology, Dalian 116024, Liaoning, People's Republic of China.
Yangyang YangSchool of Life Science and Biotechnology, Dalian University of Technology, Dalian 116024, Liaoning, People's Republic of China.
Min ChenSchool of Life Science and Biotechnology, Dalian University of Technology, Dalian 116024, Liaoning, People's Republic of China.
Xiao JiangSchool of Life Science and Biotechnology, Dalian University of Technology, Dalian 116024, Liaoning, People's Republic of China.
Huijian WuSchool of Life Science and Biotechnology, Dalian University of Technology, Dalian 116024, Liaoning, People's Republic of China.
Dalian University · CNDalian University of Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant estrogen receptor-α (ERα) signaling is recognized as a major contributor to the development of breast cancer. However, the molecular mechanism underlying the regulation of ERα in breast cancer is still inconclusive. In this study, we showed that the transcription factor 21 (TCF21) interacted with ERα, and repressed its transcriptional activity in a HDACs-dependent manner. We also showed that TCF21 could be sumoylated by the small ubiquitin-like modifier SUMO1, and this modification could be reversed by SENP1. Sumoylation of TCF21 occurred at lysine residue 24 (K24). Substitution of K24 with arginine resulted in complete abolishment of sumoylation. Sumoylation stabilized TCF21, but did not affect its subcellular localization. Sumoylation of TCF21 also enhanced its interaction with HDAC1/2 without affecting its interaction with ERα. Moreover, sumoylation of TCF21 promoted its repression of ERα transcriptional activity, and increased the recruitment of HDAC1/2 to the pS2 promoter. Consistent with these observations, sumoylation of TCF21 could inhibit the growth of ERα-positive breast cancer cells and decreased the proportion of S-phase cells in the cell cycle. These findings suggested that TCF21 might act as a negative regulator of ERα, and its sumoylation inhibited the transcriptional activity of ERα through promoting the recruitment of HDAC1/2.

Indexed as

Protein Processing, Post-TranslationalApoptosisBasic Helix-Loop-Helix ProteinsBiomarkers, TumorBreast NeoplasmsCell ProliferationDown-RegulationEstrogen Receptor alphaFemaleHistone Deacetylase 1HumansPromoter Regions, GeneticSignal TransductionSUMO-1 ProteinSumoylationTranscriptional ActivationBasic Helix-Loop-Helix ProteinsBiomarkers, TumorESR1 protein, humanEstrogen Receptor alphaHDAC1 protein, humanHistone Deacetylase 1SUMO-1 ProteinTCF21 protein, humanERαproliferationsumoylationTCF21transcriptional activity

Identifiers

PMID27028856
PMCPMC5041976
OpenAlexW2328783847

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.