Evidence map›Paper›PMID 30375428›Full record

ArticleScientific reports2018

A novel somatic mutation of SIN3A detected in breast cancer by whole-exome sequencing enhances cell proliferation through ERα expression.

Kenji Watanabe, Shigeru Yamamoto, Syuiti Sakaguti, Keishiro Isayama, Masaaki Oka, Hiroaki Nagano, Yoichi Mizukami

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
  2. ReducediScience · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Structure of a SIN3-HDAC complex from budding yeast.Nature structural & molecular biology · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Mutations ofJournal of clinical and translational research · 2021
    Article
  15. Article
  16. 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 1 institution in 1 country.

Kenji WatanabeInstitute of Gene Research, Yamaguchi University Science Research Center, Yamaguchi, 755-8505, Japan.
Shigeru YamamotoDepartment of Gastroenterological, Breast and Endocrine Surgery, Yamaguchi University Graduate School of Medicine, Yamaguchi, 755-8505, Japan.
Syuiti SakagutiInstitute of Radioisotope Research and Education, Yamaguchi University Science Research Center, Yamaguchi, 755-8505, Japan.
Keishiro IsayamaInstitute of Life Science, Yamaguchi University Science Research Center, Yamaguchi, 755-8505, Japan.
Masaaki OkaDepartment of Gastroenterological, Breast and Endocrine Surgery, Yamaguchi University Graduate School of Medicine, Yamaguchi, 755-8505, Japan.
Hiroaki NaganoDepartment of Gastroenterological, Breast and Endocrine Surgery, Yamaguchi University Graduate School of Medicine, Yamaguchi, 755-8505, Japan.
Yoichi MizukamiInstitute of Gene Research, Yamaguchi University Science Research Center, Yamaguchi, 755-8505, Japan. mizukami@yamaguchi-u.ac.jp.
Yamaguchi University · JP

Funding

Japan Science and Technology Agency (JST) 15K08210
6 · The paper itself

Abstract

Breast cancer is the most frequent tumor in women, and in nearly two-thirds of cases, the tumors express estrogen receptor α (ERα, encoded by ESR1). Here, we performed whole-exome sequencing of 16 breast cancer tissues classified according to ESR1 expression and 12 samples of whole blood, and detected 310 somatic mutations in cancer tissues with high levels of ESR1 expression. Of the somatic mutations validated by a different deep sequencer, a novel nonsense somatic mutation, c.2830 C>T; p.Gln944*, in transcriptional regulator switch-independent 3 family member A (SIN3A) was detected in breast cancer of a patient. Part of the mutant protein localized in the cytoplasm in contrast to the nuclear localization of ERα, and induced a significant increase in ESR1 mRNA. The SIN3A mutation obviously enhanced MCF7 cell proliferation. In tissue sections from the breast cancer patient with the SIN3A c.2830 C>T mutation, cytoplasmic SIN3A localization was detected within the tumor regions where nuclear enlargement was observed. The reduction in SIN3A mRNA correlates with the recurrence of ER-positive breast cancers on Kaplan-Meier plots. These observations reveal that the SIN3A mutation has lost its transcriptional repression function due to its cytoplasmic localization, and that this repression may contribute to the progression of breast cancer.

Indexed as

AdultAgedAged, 80 and overBreast NeoplasmsCell ProliferationDisease-Free SurvivalEstrogen Receptor alphaExome SequencingFemaleGene Expression Regulation, NeoplasticHumansKaplan-Meier EstimateMCF-7 CellsMiddle AgedMutationNeoplasm Recurrence, LocalESR1 protein, humanEstrogen Receptor alphaRepressor ProteinsRNA, MessengerSIN3A transcription factorSin3 Histone Deacetylase and Corepressor Complex

Identifiers

PMID30375428
PMCPMC6207735
OpenAlexW2898502896

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.