Histone deacetylases and cancer

Glozak, Michele A.; Seto, Edward

doi:10.1038/sj.onc.1210610

Cited by 921 publications

(816 citation statements)

References 119 publications

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“…By removal of acetyl groups from histones, HDACs create a non-permissive chromatin conformation that prevents the transcription of genes that encode proteins involved in tumorigenesis. In addition to histones, HDACs bind to and deacetylate a variety of other protein targets including transcription factors and other abundant cellular proteins implicated in control of cell growth, differentiation and apoptosis (Glozak and Seto, 2007). Theses findings may explain the inhibitory effects of oxcarbazepine on the proliferation of the three cancer cells used in the current study by different rates although its least activity against HepG2 cells .…”

Section: Discussionmentioning

confidence: 68%

Possible Anticancer Activity of Rosuvastatine, Doxazosin, Repaglinide and Oxcarbazepin

Sharkawi¹,

Shemy²,

Khaled³

2014

Asian Pacific Journal of Cancer Prevention

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Section: Discussionmentioning

confidence: 68%

Possible Anticancer Activity of Rosuvastatine, Doxazosin, Repaglinide and Oxcarbazepin

Sharkawi¹,

Shemy²,

Khaled³

2014

Asian Pacific Journal of Cancer Prevention

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“…Aberrant HDAC expression initiates tumor progression by causing uncontrolled cell proliferation and blocking the transcription of differentiation and proapoptotic factors [19]. HDACis, which are known differentiating compounds, restore the normal gene expression of cancer cells by altering transcription levels of cell cycle regulatory proteins; they induce the expression of the antiproliferative gene p21, regulate the activity of the tumor suppressor p53, and reduce the expression of positive regulators of proliferation, such as cyclin D1, c-myc and c-Src [17,18].…”

Section: Discussionmentioning

confidence: 99%

“…Expression of PMCA 2, 3 and 4 isoforms were 4 enhanced during differentiation of the neuroblastoma cell line IMR-32, and this resulted in increased Ca 2+ efflux [16]. Short chain fatty acids (SCFAs) are histone deacetylase inhibitors that can inhibit proliferation of tumor cells, induce differentiation and apoptosis [17][18][19][20][21][22][23][24].…”

Section: Introductionmentioning

confidence: 99%

Histone deacetylase inhibitor- and PMA-induced upregulation of PMCA4b enhances Ca2+ clearance from MCF-7 breast cancer cells

et al. 2014

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The expression of the plasma membrane Ca 2+ ATPase (PMCA) isoforms is altered in several types of cancer cells suggesting that they are involved in cancer progression. In this study we induced differentiation of MCF-7 breast cancer cells by histone deacetylase inhibitors (HDACis) such as short chain fatty acids (SCFAs) or suberoylanilide hydroxamic acid (SAHA), and by phorbol 12-myristate 13-acetate (PMA) and found strong upregulation of PMCA4b protein expression in response to these treatments. Furthermore, combination of HDACis with PMA augmented cell differentiation and further enhanced PMCA4b expression both at mRNA and protein levels. Immunocytochemical analysis revealed that the upregulated protein was located mostly in the plasma membrane. To examine the functional consequences of elevated PMCA4b expression, the characteristics of intracellular Ca 2+ signals were investigated before and after differentiation inducing treatments, and also in cells overexpressing PMCA4b. The increased PMCA4b expression -either by treatment or overexpression -led to enhanced Ca 2+ clearance from the stimulated cells. We found pronounced PMCA4 protein expression in normal breast tissue samples highlighting the importance of this pump for the maintenance of mammary epithelial Ca 2+ homeostasis. These results suggest that modulation of Ca 2+ signaling by enhanced PMCA4b expression may contribute to normal development of breast epithelium and may be lost in cancer.3

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“…Lysine acetylation and methylation are both reversible processes thanks to the activities of histone deacetylases and recently discovered demethylases [1,4]. Both of these enzyme families are implicated in a range of developmental and physiologic pathways as well as in malignancy [1,5,6].…”

Section: Introductionmentioning

confidence: 99%

Chromatin state maps: new technologies, new insights

Mendenhall

Bernstein

2008

Current Opinion in Genetics & Development

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Recent years have seen unprecedented characterization of mammalian chromatin thanks to advances in chromatin assays, antibody development and genomics. Genome-wide maps of chromatin state can now be readily acquired using microarrays or next-generation sequencing technologies. These datasets reveal local and long-range chromatin patterns that offer insight into the locations and functions of underlying regulatory elements and genes. These patterns are dynamic across developmental stages and lineages. Global studies of chromatin in embryonic stem cells have led to intriguing hypotheses regarding Polycomb/trithorax and RNA polymerase roles in 'poising' transcription. Chromatin state maps thus provide a rich resource for understanding chromatin at a 'systems level', and a starting point for mechanistic studies aimed at defining epigenetic controls that underlie development.

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Histone deacetylases and cancer

Cited by 921 publications

References 119 publications

Possible Anticancer Activity of Rosuvastatine, Doxazosin, Repaglinide and Oxcarbazepin

Possible Anticancer Activity of Rosuvastatine, Doxazosin, Repaglinide and Oxcarbazepin

Histone deacetylase inhibitor- and PMA-induced upregulation of PMCA4b enhances Ca2+ clearance from MCF-7 breast cancer cells

Chromatin state maps: new technologies, new insights

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