Evidence map›Paper›PMID 31081251›Full record

ArticleMolecular oncology2019

HDAC7-mediated control of tumour microenvironment maintains proliferative and stemness competence of human mammary epithelial cells.

Valentina Cutano, Eros Di Giorgio, Martina Minisini, Raffaella Picco, Emiliano Dalla, Claudio Brancolini

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.4field-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

29 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
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  7. HDAC7 promotes ovarian cancer malignancy via AKT/mTOR signalling pathway.Journal of cellular and molecular medicine · 2024
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  16. Differential molecular mechanistic behavior of HDACs in cancer progression.Medical oncology (Northwood, London, England) · 2022
    Review
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  19. Article
  20. MiR-342-3p inhibits LCSC oncogenicity and cell stemness through HDAC7/PTEN axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    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

6 authors at 1 institution in 1 country.

Valentina CutanoDepartment of Medicine, Università degli Studi di Udine, Italy.
Eros Di GiorgioDepartment of Medicine, Università degli Studi di Udine, Italy.
Martina MinisiniDepartment of Medicine, Università degli Studi di Udine, Italy.
Raffaella PiccoDepartment of Medicine, Università degli Studi di Udine, Italy.
Emiliano DallaDepartment of Medicine, Università degli Studi di Udine, Italy.ORCID 0000-0002-4687-6011
Claudio BrancoliniDepartment of Medicine, Università degli Studi di Udine, Italy.ORCID 0000-0002-6597-5373
University of Udine · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HDAC7 is a pleiotropic transcriptional coregulator that controls different cellular fates. Here, we demonstrate that in human mammary epithelial cells, HDAC7 sustains cell proliferation and favours a population of stem-like cells, by maintaining a proficient microenvironment. In particular, HDAC7 represses a repertoire of cytokines and other environmental factors, including elements of the insulin-like growth factor signalling pathway, IGFBP6 and IGFBP7. This HDAC7-regulated secretome signature predicts negative prognosis for luminal A breast cancers. ChIP-seq experiments revealed that HDAC7 binds locally to the genome, more frequently distal from the transcription start site. HDAC7 can colocalize with H3K27-acetylated domains and its deletion further increases H3K27ac at transcriptionally active regions. HDAC7 levels are increased in RAS-transformed cells, in which this protein was required not only for proliferation and cancer stem-like cell growth, but also for invasive features. We show that an important direct target of HDAC7 is IL24, which is sufficient to suppress the growth of cancer stem-like cells.

Indexed as

Tumor MicroenvironmentAcetylationBone Morphogenetic Protein 4Breast NeoplasmsCell ProliferationCells, CulturedCell Transformation, NeoplasticCellular ReprogrammingEpithelial CellsFemaleGene Expression Regulation, NeoplasticHistone DeacetylasesHistonesHumansMammary Glands, HumanNeoplastic Stem CellsBone Morphogenetic Protein 4HDAC7 protein, humanHistone DeacetylasesHistonesbreast cancerCRISPR/Cas9HDAC7IL24MEF2RAS

Identifiers

PMID31081251
PMCPMC6670296
OpenAlexW2946425120

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.