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

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

doi:10.1002/1878-0261.12503

Cited by 35 publications

(45 citation statements)

References 53 publications

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“…Tar-getScan database was applied for predicting miR-489's target gene and the results showed that HDAC7 was one of the candidate target genes of miR-489. Histone deacetylase HDAC7 is proved to be involved in a variety of cellular physiological processes and as a novel target for tumor therapy [22][23][24]. Previous studies have showed that HDAC7 was involved in the malignant phenotype of glioma regulated by ZNF326 [25].…”

Section: Discussionmentioning

confidence: 99%

MiR-489 inhibited the development of gastric cancer via regulating HDAC7 and PI3K/AKT pathway

Zhang

Yuan

et al. 2020

World J Surg Onc

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Background: Mounting evidences have displayed that the dysregulation of miRNAs plays important roles in the pathogenesis of gastric cancer (GC). The purpose of this study was to explore the biological functions and potential mechanism of miR-489 in GC progression. Methods: Quantitative real-time PCR (qRT-PCR) and western blot were performed to examine the mRNA expression and protein levels of miR-489 and HDAC7. The relationship between miR-489 and HDAC7 was analyzed by Spearman rank correlation. 3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide (MTT) assay and transwell assays were conducted for determining the effect of miR-489 and HDAC7 on GC cell viability, migration, and invasion. TargetScan and luciferase reporter assay were used to confirm the target gene of miR-489 in GC cells. Results: The findings showed that miR-489 was dramatically decreased in GC tissues and GC cell lines (SGC-7901 and MKN45). Moreover, it was closely correlated with overall survival (OS) and progression-free survival (PFS) of GC patients. Downregulation of miR-489 significantly promoted GC cell proliferation, invasion, and migration. Additionally, HDAC7 was confirmed as the direct target of miR-489. Knockdown of HDAC7 exerted inhibited effect on GC progression and it markedly overturned miR-489 inhibitor-medicated effect on GC cells. More interestingly, via targeting HDAC7, miR-489 blocked the activation of PI3K/AKT pathway in GC cells. Conclusions: Correctively, miR-489 played as a tumor suppressor in GC cell growth by targeting HDAC7, and miR-489 might function as a novel biomarker for diagnosis or therapeutic targets of human GC.

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Section: Discussionmentioning

confidence: 99%

MiR-489 inhibited the development of gastric cancer via regulating HDAC7 and PI3K/AKT pathway

Zhang

Yuan

et al. 2020

World J Surg Onc

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“…The authors argued that the contribution of HDACs in the regulation of inflammation response could differ from inflammatory cells to other cell types. Indeed, deletion of HDAC9 and of other class IIa HDACs in non-inflammatory cells, similarly reported the up-regulation of some inflammatory cytokines [ 26 , 75 ]. The context-dependent effects of HDAC9 could be explained by the observation that class IIa are not required to completely abolish H3K27ac.…”

Section: Hdac9 Expression In Inflammation and In The Immune Responmentioning

confidence: 99%

Quis Custodiet Ipsos Custodes (Who Controls the Controllers)? Two Decades of Studies on HDAC9

Brancolini

Giorgio

Formisano

et al. 2021

Life

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Understanding how an epigenetic regulator drives different cellular responses can be a tricky task. Very often, their activities are modulated by large multiprotein complexes, the composition of which is context- and time-dependent. As a consequence, experiments aimed to unveil the functions of an epigenetic regulator can provide different outcomes and conclusions, depending on the circumstances. HDAC9 (histone deacetylase), an epigenetic regulator that influences different differentiating and adaptive responses, makes no exception. Since its discovery, different phenotypes and/or dysfunctions have been observed after the artificial manipulation of its expression. The cells and the microenvironment use multiple strategies to control and monitor HDAC9 activities. To date, some of the genes under HDAC9 control have been identified. However, the exact mechanisms through which HDAC9 can achieve all the different tasks so far described, remain mysterious. Whether it can assemble into different multiprotein complexes and how the cells modulate these complexes is not clearly defined. In summary, despite several cellular responses are known to be affected by HDAC9, many aspects of its network of interactions still remain to be defined.

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“…While studies are increasingly describing RIS epigenetics, detailed data about the epigenetic modifications in other types of OIS are unavailable. Additional data are desirable since increasing evidences highlight the key roles played by epigenetic regulators in maintaining OIS and counteracting oncogenic transformation [84,[111][112][113][114][115][116]. For example, in melanomas the activation of H3K9me3 demethylases (LSD1 and JMJD2C) selectively de-represses E2F target genes, allowing senescence escape and tumorigenesis [117].…”

Section: Different Types Of Ois?mentioning

confidence: 99%

The Histone Code of Senescence

Paluvai

Giorgio

Brancolini

2020

Cells

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Senescence is the end point of a complex cellular response that proceeds through a set of highly regulated steps. Initially, the permanent cell-cycle arrest that characterizes senescence is a pro-survival response to irreparable DNA damage. The maintenance of this prolonged condition requires the adaptation of the cells to an unfavorable, demanding and stressful microenvironment. This adaptation is orchestrated through a deep epigenetic resetting. A first wave of epigenetic changes builds a dam on irreparable DNA damage and sustains the pro-survival response and the cell-cycle arrest. Later on, a second wave of epigenetic modifications allows the genomic reorganization to sustain the transcription of pro-inflammatory genes. The balanced epigenetic dynamism of senescent cells influences physiological processes, such as differentiation, embryogenesis and aging, while its alteration leads to cancer, neurodegeneration and premature aging. Here we provide an overview of the most relevant histone modifications, which characterize senescence, aging and the activation of a prolonged DNA damage response.

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

Cited by 35 publications

References 53 publications

MiR-489 inhibited the development of gastric cancer via regulating HDAC7 and PI3K/AKT pathway

MiR-489 inhibited the development of gastric cancer via regulating HDAC7 and PI3K/AKT pathway

Quis Custodiet Ipsos Custodes (Who Controls the Controllers)? Two Decades of Studies on HDAC9

The Histone Code of Senescence

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