Evidence map›Paper›PMID 27780928›Full record

ArticleOncotarget2016

SIN3A and SIN3B differentially regulate breast cancer metastasis.

Monica J Lewis, Jianzhong Liu, Emily Falk Libby, Minnkyong Lee, Nigel P S Crawford, Douglas R Hurst

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 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
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  16. Soft repression: Subtle transcriptional regulation with global impact.BioEssays : news and reviews in molecular, cellular and developmental biology · 2021
    Article
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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

6 authors at 3 institutions in 1 country.

Monica J LewisDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA.
Jianzhong LiuDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA.
Emily Falk LibbyDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA.
Minnkyong LeeGenetics and Molecular Biology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA.
Nigel P S CrawfordGenetics and Molecular Biology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA.
Douglas R HurstDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA.
University of Alabama at Birmingham · USNational Human Genome Research Institute · USNational Institutes of Health · US

Funding

XRAY CRYSTALLOGRAPHYP30CA013148 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Robert S Welner · 1985 to 2026
$165.9M
Cancer Prevention & Control Training ProgramR25CA047888 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DEMARK-WAHNEFRIED, WENDY, MENESES, KAREN M · 1988 to 2016
$11.2M
NCI NIH HHS P30 CA013148NCI NIH HHS R25 CA047888
6 · The paper itself

Abstract

SIN3 corepressor complexes play important roles in both normal development and breast cancer. Mammalian cells have two paralogs of SIN3 (SIN3A and SIN3B) that are encoded by distinct genes and have unique functions in many developmental processes. However, specific roles for SIN3A and SIN3B in breast cancer progression have not been characterized. We generated stable knockdown cells of SIN3 paralogs individually and in combination using three non-overlapping shRNA. Stable knockdown of SIN3B caused a significant decrease in transwell invasion through Matrigel and decreased the number of invasive colonies when grown in a 3D extracellular matrix. Conversely, stable knockdown of SIN3A significantly increased transwell invasion and increased the number of invasive colonies. These results were corroborated in vivo in which SIN3B knockdown significantly decreased and SIN3A knockdown increased experimental lung metastases. RNA sequencing was used to identify unique targets and biological pathways that were altered upon knockdown of SIN3A compared to SIN3B. Additionally, we analyzed microarray data sets to identify correlations of SIN3A and SIN3B expression with survival in patients with breast cancer. These data sets indicated that high mRNA expression of SIN3A as well as low mRNA expression of SIN3B correlates with longer relapse free survival specifically in patients with triple negative breast cancer which corresponds with our in vitro and in vivo data. These results demonstrate key functional differences between SIN3 paralogs in regulating the process of breast cancer metastasis and suggest metastasis suppressive roles of SIN3A and metastasis promoting roles of SIN3B.

Indexed as

Cell MovementAnimalsCell Line, TumorCell ProliferationDisease-Free SurvivalDisease ProgressionFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticGene Regulatory NetworksHumansKaplan-Meier EstimateLung NeoplasmsMice, NudeNeoplasm InvasivenessNeoplasm Recurrence, LocalRepressor ProteinsRNA, MessengerSIN3A transcription factorSIN3B protein, humanSin3 Histone Deacetylase and Corepressor Complexbreast cancerinvasionmetastasisSIN3ASIN3B

Identifiers

PMID27780928
PMCPMC5340233
OpenAlexW2538285028

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.