The histone demethylase LSD1 is required for estrogen-dependent S100A7 gene expression in human breast cancer cells

Yu, Seung Eun; Jang, Yong Suk

doi:10.1016/j.bbrc.2012.09.057

Cited by 10 publications

(11 citation statements)

References 24 publications

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“…Colony formation assay was performed as in the previous report (29). For colony formation assay, cells were seeded at 1 × 10 3 cells per well in 60 mm dishes in triplicate and maintained for 14 days.…”

Section: Methodsmentioning

confidence: 99%

CDK2-dependent phosphorylation of Suv39H1 is involved in control of heterochromatin replication during cell cycle progression

Park

Chai

et al. 2014

Nucleic Acids Research

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Although several studies have suggested that the functions of heterochromatin regulators may be regulated by post-translational modifications during cell cycle progression, regulation of the histone methyltransferase Suv39H1 is not fully understood. Here, we demonstrate a direct link between Suv39H1 phosphorylation and cell cycle progression. We show that CDK2 phosphorylates Suv39H1 at Ser391 and these phosphorylation levels oscillate during the cell cycle, peaking at S phase and maintained during S-G2-M phase. The CDK2-mediated phosphorylation of Suv39H1 at Ser391 results in preferential dissociation from chromatin. Furthermore, phosphorylation-mediated dissociation of Suv39H1 from chromatin causes an enhanced occupancy of JMJD2A histone demethylase on heterochromatin and alterations in inactive histone marks. Overexpression of phospho-mimic Suv39H1 induces early replication of heterochromatin, suggesting the importance of Suv39H1 phosphorylation in the replication of heterochromatin. Moreover, overexpression of phospho-defective Suv39H1 caused altered replication timing of heterochromatin and increases sensitivity to replication stress. Collectively, our data suggest that phosphorylation-mediated modulation of Suv39H1-chromatin association may be an initial step in heterochromatin replication.

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Section: Methodsmentioning

confidence: 99%

CDK2-dependent phosphorylation of Suv39H1 is involved in control of heterochromatin replication during cell cycle progression

Park

Chai

et al. 2014

Nucleic Acids Research

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“…64 The method is highly applied in clinical studies, since only small cell numbers are required. Yu et al 65 observed, upon LSD1 inhibition with pargyline in MCF-7 breast cancer cells, significantly reduced E2-mediated S100A7 expression. In addition, differentiation markers can be epigenetically regulated and be examined via FACS.…”

Section: Protein Analysis Invasion Assay Reporter Assaymentioning

confidence: 99%

Cellular analysis of the action of epigenetic drugs and probes

et al. 2017

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Small molecule drugs and probes are important tools in drug discovery, pharmacology, and cell biology. This is of course also true for epigenetic inhibitors. Important examples for the use of established epigenetic inhibitors are the study of the mechanistic role of a certain target in a cellular setting or the modulation of a certain phenotype in an approach that aims toward therapeutic application. Alternatively, cellular testing may aim at the validation of a new epigenetic inhibitor in drug discovery approaches. Cellular and eventually animal models provide powerful tools for these different approaches but certain caveats have to be recognized and taken into account. This involves both the selectivity of the pharmacological tool as well as the specificity and the robustness of the cellular system. In this article, we present an overview of different methods that are used to profile and screen for epigenetic agents and comment on their limitations. We describe not only diverse successful case studies of screening approaches using different assay formats, but also some problematic cases, critically discussing selected applications of these systems.

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“…Estrogen‐mediated S100A7 expression facilitated by LSD1 may prevent breast cancer cell propagation, suggesting a possible tumor suppressor‐like role for S100A7 and that this action is intervened by LSD1 in ER‐positive breast cancer cells. The controversy role of LSD1 on ER‐positive or ER‐negative breast cancer cells as well as whether LSD1 can be recognized as an effective anticancer therapeutic target in breast cancer needs to be investigated in the future …”

Section: Physiological and Pathophysiological Functions Of Lsd1mentioning

confidence: 99%

“…It was reported that LSD1 was overexpressed in numerous kinds of tumors, containing gastric cancer, esophageal cancer, breast cancer, lung cancer, colon cancer, prostate cancer, and bladder cancer . In these either hormone‐dependent or hormone‐independent cancers, LSD1 plays a vital role in promoting cell proliferation and development; meanwhile, LSD1 also promotes cell migration, cell invasion, and metastasis by introducing EMT .…”

Section: Physiological and Pathophysiological Functions Of Lsd1mentioning

confidence: 99%

A Systematic Review of Histone Lysine‐Specific Demethylase 1 and Its Inhibitors

Zheng¹,

Wang²,

Li³

et al. 2015

Medicinal Research Reviews

164

130

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Histone lysine-specific demethylase 1 (LSD1) is the first discovered and reported histone demethylase by Dr. Shi Yang's group in 2004. It is classified as a member of amine oxidase superfamily, the common feature of which is using the flavin adenine dinucleotide (FAD) as its cofactor. Since it is located in cell nucleus and acts as a histone methylation eraser, LSD1 specifically removes mono- or dimethylated histone H3 lysine 4 (H3K4) and H3 lysine 9 (H3K9) through formaldehyde-generating oxidation. It has been indicated that LSD1 and its downstream targets are involved in a wide range of biological courses, including embryonic development and tumor-cell growth and metastasis. LSD1 has been reported to be overexpressed in variety of tumors. Inactivating LSD1 or downregulating its expression inhibits cancer-cell development. LSD1 targeting inhibitors may represent a new insight in anticancer drug discovery. This review summarizes recent studies about LSD1 and mainly focuses on the basic physiological function of LSD1 and its involved mechanisms in pathophysiologic conditions, as well as the development of LSD1 inhibitors as potential anticancer therapeutic agents.

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The histone demethylase LSD1 is required for estrogen-dependent S100A7 gene expression in human breast cancer cells

Cited by 10 publications

References 24 publications

CDK2-dependent phosphorylation of Suv39H1 is involved in control of heterochromatin replication during cell cycle progression

CDK2-dependent phosphorylation of Suv39H1 is involved in control of heterochromatin replication during cell cycle progression

Cellular analysis of the action of epigenetic drugs and probes

A Systematic Review of Histone Lysine‐Specific Demethylase 1 and Its Inhibitors

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