Histone deacetylase inhibition redistributes topoisomerase IIb from heterochromatin to euchromatin

Cowell, Ian G.; Papageorgiou, Nikolaos S.; Padget, Kay; Watters, Gary P.; Austin, Caroline A.

doi:10.4161/nucl.2.1.14194

Cited by 19 publications

(16 citation statements)

References 52 publications

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“…The same immunoprecipitates and in vitro incubation conditions did not decrease the topoisomerase IIβ complexes, in fact the immunofluorescent signal increased. This may be due to increased accessibility to the anti-topoisomerase IIβ antisera following detergent and salt treatment of heterochromatin (Cowell et al, 2011b). Etoposide stabilised topoisomerase II adducts were also removed from genomic DNA in vitro by recombinant MRE11, 49% of the topoisomerase IIα adducts were removed ( P >0.0001), but only 7% of the topoisomerase IIβ complexes (p = 0.0302).…”

Section: Discussionmentioning

confidence: 99%

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MRE11 facilitates the removal of human topoisomerase II complexes from genomic DNA

et al. 2012

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SummaryTopoisomerase II creates a double-strand break intermediate with topoisomerase covalently coupled to the DNA via a 5′-phosphotyrosyl bond. These intermediate complexes can become cytotoxic protein-DNA adducts and DSB repair at these lesions requires removal of topoisomerase II. To analyse removal of topoisomerase II from genomic DNA we adapted the trapped in agarose DNA immunostaining assay. Recombinant MRE11 from 2 sources removed topoisomerase IIα from genomic DNA in vitro, as did MRE11 immunoprecipitates isolated from A-TLD or K562 cells. Basal topoisomerase II complex levels were very high in A-TLD cells lacking full-length wild type MRE11, suggesting that MRE11 facilitates the processing of topoisomerase complexes that arise as part of normal cellular metabolism. In K562 cells inhibition of MRE11, PARP or replication increased topoisomerase IIα and β complex levels formed in the absence of an anti-topoisomerase II drug.

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Section: Discussionmentioning

confidence: 99%

“…Immunofluorescence was carried out essentially as described by Cowell et al, 2011b. MRE11 immunofluorescence was carried out using rabbit anti-AB397 (Abcam).…”

Section: Methodsmentioning

confidence: 99%

MRE11 facilitates the removal of human topoisomerase II complexes from genomic DNA

et al. 2012

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“…Histone deacetylases are a class of enzymes deacetylating the acetyl group from ε-N-acetyl lysine amino acid from a histone, which lead to the tight wrapping of DNA. HDACs play a key role in the homeostasis maintenances of histone acetylation euchromatin and heterochromatin in living system 9 , 10 . There are 18 HDACs recognized up to now, divided into HDAC I (HDAC 1, 2, and 3: mainly in the nucleus; HDAC 8: partially in the cytoplasm), HDAC II (HDAC 4, 5, 6, 7, 9, and 10: shuttling in and out of the nucleus), as Table 1 showed 11 .…”

Section: Histone Deacetylases (Hdacs)mentioning

confidence: 99%

Histone Deacetylases (HDACs) Guided Novel Therapies for T-cell lymphomas

et al. 2019

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T-cell lymphomas are a heterogeneous group of cancers with different pathogenesis and poor prognosis. Histone deacetylases (HDACs) are epigenetic modifiers that modulate many key biological processes. In recent years, HDACs have been fully investigated for their roles and potential as drug targets in T-cell lymphomas. In this review, we have deciphered the modes of action of HDACs, HDAC inhibitors as single agents, and HDACs guided combination therapies in T-cell lymphomas. The overview of HDACs on the stage of T-cell lymphomas, and HDACs guided therapies both as single agents and combination regimens endow great opportunities for the cure of T-cell lymphomas.

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“…As shown in Figure 1, the fluorescent-labeled monoclonal Ki-67 antibody has been used for cell cycle measurement and cancer diagnosis. Other commonly used cell proliferation biomarkers include proliferating cell nuclear antigen PCNA [29], topoisomerase IIB [30], and phosphorylated histone H3 [31].…”

Section: Protein Biomarkersmentioning

confidence: 99%

Cell Growth Measurement

Chen¹,

Rui²,

Yu³

et al. 2020

Cell Growth

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The cell is the basic structural and functional unit of all living organisms. As the smallest unit and building blocks of life, cells differ in size, shape, metabolism, reproduction, and growth requirements. Cells reproduce through cell division involving a four-phase (G1, S, G2, M) cell cycle, which is tightly regulated at multiple checkpoints. The resulting growth curve demonstrates that cell population increases in three sequential steps: incubation, exponential hyperplasia, and stagnation/death phases. Cell growth is subject to changes in disease state and/or environmental conditions. This chapter will focus on methods for cell growth measurement, which are grouped into five sections: cell cycle, apoptosis, growth curve, druginduced proliferation (DIP), and continuous assays. Among the continuous assays, the EZMTT dye allows for long-term tracking of cell growth under various conditions and shows promise in precision medicine by early detection of drug resistance.

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Histone deacetylase inhibition redistributes topoisomerase IIb from heterochromatin to euchromatin

Cited by 19 publications

References 52 publications

MRE11 facilitates the removal of human topoisomerase II complexes from genomic DNA

MRE11 facilitates the removal of human topoisomerase II complexes from genomic DNA

Histone Deacetylases (HDACs) Guided Novel Therapies for T-cell lymphomas

Cell Growth Measurement

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