Evidence map›Paper›PMID 27779108›Full record

ArticleOncotarget2016

RNAi screens identify CHD4 as an essential gene in breast cancer growth.

Carolina D'Alesio, Simona Punzi, Angelo Cicalese, Lorenzo Fornasari, Laura Furia, Laura Riva, Alessandro Carugo, Giuseppe Curigliano, Carmen Criscitiello, Giancarlo Pruneri and 4 more

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.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.6field-weighted citation impact, top 10% 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, 44 citations in OpenAlex.

  1. Article
  2. Animals : an open access journal from MDPI · 2025
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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

14 authors at 3 institutions in 2 countries.

Carolina D'AlesioDepartment of Experimental Oncology, European Institute of Oncology, Milan 20141, Italy.
Simona PunziDepartment of Experimental Oncology, European Institute of Oncology, Milan 20141, Italy.
Angelo CicaleseDepartment of Experimental Oncology, European Institute of Oncology, Milan 20141, Italy.
Lorenzo FornasariDepartment of Experimental Oncology, European Institute of Oncology, Milan 20141, Italy.
Laura FuriaDepartment of Experimental Oncology, European Institute of Oncology, Milan 20141, Italy.
Laura RivaCenter for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia, Milan 20139, Italy.
Alessandro CarugoDepartment of Experimental Oncology, European Institute of Oncology, Milan 20141, Italy.
Giuseppe CuriglianoDivision of Experimental Therapeutics, European Institute of Oncology, Milan 20141, Italy.
Carmen CriscitielloDivision of Experimental Therapeutics, European Institute of Oncology, Milan 20141, Italy.
Giancarlo PruneriSchool of Medicine, University of Milan, Milan 20122, Italy.
Pier Giuseppe PelicciDepartment of Experimental Oncology, European Institute of Oncology, Milan 20141, Italy.
Mario FarettaDepartment of Experimental Oncology, European Institute of Oncology, Milan 20141, Italy.
Daniela BossiDepartment of Experimental Oncology, European Institute of Oncology, Milan 20141, Italy.
Luisa LanfranconeDepartment of Experimental Oncology, European Institute of Oncology, Milan 20141, Italy.
European Institute of Oncology · ITCenter for Genomic Science · ITUniversity of Milan · IT

Funding

European Research Council 341131
6 · The paper itself

Abstract

Epigenetic regulation plays an essential role in tumor development and epigenetic modifiers are considered optimal potential druggable candidates. In order to identify new breast cancer vulnerabilities and improve therapeutic chances for patients, we performed in vivo and in vitro shRNA screens in a human breast cancer cell model (MCF10DCIS.com cell line) using epigenetic libraries. Among the genes identified in our screening, we deeply investigated the role of Chromodomain Helicase DNA binding Protein 4 (CHD4) in breast cancer tumorigenesis. CHD4 silencing significantly reduced tumor growth in vivo and proliferation in vitro of MCF10DCIS.com cells. Similarly, in vivo breast cancer growth was decreased in a spontaneous mouse model of breast carcinoma (MMTV-NeuT system) and in metastatic patient-derived xenograft models. Conversely, no reduction in proliferative ability of non-transformed mammary epithelial cells (MCF10A) was detected. Moreover, we showed that CHD4 depletion arrests proliferation by inducing a G0/G1 block of cell cycle associated with up-regulation of CDKN1A (p21). These results highlight the relevance of genetic screens in the identification of tumor frailties and the role of CHD4 as a potential pharmacological target to inhibit breast cancer growth.

Indexed as

Cell ProliferationRNA InterferenceAnimalsBreast NeoplasmsCell Cycle CheckpointsCell Line, TumorComputational BiologyCyclin-Dependent Kinase Inhibitor p21DNA HelicasesFemaleGene Expression Regulation, NeoplasticGene LibraryGene Regulatory NetworksGenetic Predisposition to DiseaseHumansMi-2 Nucleosome Remodeling and Deacetylase ComplexCDKN1A protein, humanCdkn1a protein, mouseCHD4 protein, humanCyclin-Dependent Kinase Inhibitor p21DNA HelicasesMi-2beta protein, mouseMi-2 Nucleosome Remodeling and Deacetylase Complexbreast cancerCHD4epigenetic targetsin vivo murine and human modelsRNAi screen

Identifiers

PMID27779108
PMCPMC5348363
OpenAlexW2530246084

What OpenQuestion holds

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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.