Evidence map›Paper›PMID 27429856›Full record

ArticleAmerican journal of cancer research2016

Breast cancer metastasis suppressor 1 modulates SIRT1-dependent p53 deacetylation through interacting with DBC1.

Xueni Liu, Elphire Ehmed, Boyao Li, Jianming Dou, Xiaojing Qiao, Wenyong Jiang, Xi Yang, Shouyi Qiao, Yanhua Wu

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 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
2.1field-weighted citation impact, top 13% 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, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Deacetylation of Transcription Factors in Carcinogenesis.International journal of molecular sciences · 2021
    Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Loss of DBC1 (CCAR2) affects TNFα-induced lipolysis andJournal of molecular endocrinology · 2018
    Article
  10. Article
  11. Article
  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

9 authors at 1 institution in 1 country.

Xueni LiuState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University Shanghai 200438, P. R. China.
Elphire EhmedState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University Shanghai 200438, P. R. China.
Boyao LiState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University Shanghai 200438, P. R. China.
Jianming DouState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University Shanghai 200438, P. R. China.
Xiaojing QiaoState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University Shanghai 200438, P. R. China.
Wenyong JiangState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University Shanghai 200438, P. R. China.
Xi YangState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University Shanghai 200438, P. R. China.
Shouyi QiaoState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University Shanghai 200438, P. R. China.
Yanhua WuState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University Shanghai 200438, P. R. China.
Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer metastasis suppressor 1 (BRMS1) is a specific tumor metastasis suppressor implicated in the regulation of chromatin modification and gene transcription. However, the molecular mechanism of BRMS1 remains to be elucidated. Here, we report that DBC1 (deleted in breast cancer 1), is a novel interacting protein of BRMS1. The imperfect leucine zipper motifs of BRMS1 and the N-terminal domain of DBC1 are required for the interaction. DBC1 is identified as an important negative regulator of SIRT1's activity and genotoxic stress response. We demonstrated that BRMS1 is able to interrupt endogenous DBC1-SIRT1 association. Consistently, SIRT1-dependent p53 acetylation under genotoxic stress is also affected by BRMS1. Overall, our results identify BRMS1 as a novel regulator of DBC1-SIRT1 complex and SIRT1-dependent p53 deacetylation.

Indexed as

BRMS1DBC1p53protein interactionSIRT1

Identifiers

PMID27429856
PMCPMC4937745
OpenAlexW2492384528

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.