Dysregulation of different modes of programmed cell death by epigenetic modifications and their role in cancer

Damiescu, R.; Efferth, T.; Dawood, M.

doi:10.1016/j.canlet.2024.216623

Cited by 4 publications

(4 citation statements)

References 129 publications

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“…DNA methylation, histone modification and non-coding RNAs modification affect various patterns of cell death [ 77 ]. DNA methylation can modulate autophagy and tumour growth by regulating the expression of autophagy genes such as Beclin-1, ATG4A and ELFN2.…”

Section: Molecular Mechanisms Of Different Cell Death Pathwaysmentioning

confidence: 99%

“…DNA methylation can modulate autophagy and tumour growth by regulating the expression of autophagy genes such as Beclin-1, ATG4A and ELFN2. In addition, histone acetylation and dysregulation of non-coding RNAs mediated autophagy have been associated with different kinds of cancers [ 77 , 78 ]. DNA methylation and histone phosphorylation regulate apoptosis by modulating the expression of apoptosis-related genes including P53, BAX and Caspase-8 [ 79 ].…”

Section: Molecular Mechanisms Of Different Cell Death Pathwaysmentioning

confidence: 99%

“…DNA methylation and histone phosphorylation regulate apoptosis by modulating the expression of apoptosis-related genes including P53, BAX and Caspase-8 [ 79 ]. DNA methylation regulates ferroptosis-related genes such as SCD1 and FADS2 to suppress ferroptosis and histone acetyltransferases inhibit ferroptosis by regulating GSH production [ 77 ]. The lymphocyte-specific deconjugation enzymes, which modify P53 via chromatin modification, histones and non-coding RNAs all affect expression of SLC7A11, thus induce ferroptosis [ 80 ], even the possibility of regulating disulfidptosis is further suspected.…”

Section: Molecular Mechanisms Of Different Cell Death Pathwaysmentioning

confidence: 99%

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Epigenetic regulation of diverse cell death modalities in cancer: a focus on pyroptosis, ferroptosis, cuproptosis, and disulfidptosis

Zhou,

Liu,

Wan

et al. 2024

J Hematol Oncol

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Tumor is a local tissue hyperplasia resulted from cancerous transformation of normal cells under the action of various physical, chemical and biological factors. The exploration of tumorigenesis mechanism is crucial for early prevention and treatment of tumors. Epigenetic modification is a common and important modification in cells, including DNA methylation, histone modification, non-coding RNA modification and m6A modification. The normal mode of cell death is programmed by cell death-related genes; however, recent researches have revealed some new modes of cell death, including pyroptosis, ferroptosis, cuproptosis and disulfidptosis. Epigenetic regulation of various cell deaths is mainly involved in the regulation of key cell death proteins and affects cell death by up-regulating or down-regulating the expression levels of key proteins. This study aims to investigate the mechanism of epigenetic modifications regulating pyroptosis, ferroptosis, cuproptosis and disulfidptosis of tumor cells, explore possible triggering factors in tumor development from a microscopic point of view, and provide potential targets for tumor therapy and new perspective for the development of antitumor drugs or combination therapies.

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Section: Molecular Mechanisms Of Different Cell Death Pathwaysmentioning

confidence: 99%

Section: Molecular Mechanisms Of Different Cell Death Pathwaysmentioning

confidence: 99%

Section: Molecular Mechanisms Of Different Cell Death Pathwaysmentioning

confidence: 99%

See 1 more Smart Citation

Epigenetic regulation of diverse cell death modalities in cancer: a focus on pyroptosis, ferroptosis, cuproptosis, and disulfidptosis

Zhou,

Liu,

Wan

et al. 2024

J Hematol Oncol

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“…Uncommon DNA methylation can result in the tumor suppressor genes silencing, essential guardians of cellular integrity and regulators of cell growth, division, and apoptosis. Conversely, it can lead to the activation of oncogenes, with cell proliferation and survival enhancement, contributing to malignant transformation (5,6) . Similarly, perturbations in histone modifications, such as H3K27me3 catalyzed by EZH2 (7) and H4R3me2s mediated by PRMT5 (8) , play pivotal roles in driving these epigenetic alterations in cancer cells.…”

Section: Introductionmentioning

confidence: 99%

Ellagic acid: a potential inhibitor of enhancer of zeste homolog-2 and protein arginine methyltransferase-5

Nalla,

Chatterjee,

Poyya

et al. 2024

Preprint

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Dysregulation of epigenetic processes, characterized by aberrant DNA methylation patterns and histone modifications, is a hallmark of cancer, driving its initiation, progression, and metastasis by silencing tumor suppressor genes or activating oncogenes. Perturbations in histone modifications such as H3K27me3 by EZH2 and H4R3me2s by PRMT5 play significant roles in these epigenetic alterations, disrupting normal gene expression and facilitating oncogene activation while suppressing tumor suppressor genes. Consequently, inhibitors targeting enzymes involved in DNA methylation, histone modification, or chromatin remodeling, such as PRMTs and PRC complexes, are promising anti-cancer agents, with several undergoing pre-clinical and clinical trials. Our screening of a phytochemical library revealed ellagic acid as an effective inhibitor of both EZH2 and PRMT5. Ellagic acid interacts strongly with the EZH2 and PRMT5:MEP50 complex, binding to their active sites through π-cation interactions and hydrogen bonds. Surface Plasmon Resonance study confirmed potent binding affinities of ellagic acid, with KD values of 3.28E-06 and 6.54E-05 for EZH2 and PRMT5:MEP50 respectively. In-vitro assays validated inhibitory effects on EZH2 and PRMT5:MEP50 by reducing the levels of their catalytic products H3K27me3 and H4R3me2s respectively and induction of autophagy and apoptosis. Further In-vivo studies using mouse xenografts further demonstrated significant tumor size reductions upon oral administration of ellagic acid, with decreased expression of the proliferative marker ki67 and histone repressive marks. Taken together we showed that inhibition of EZH2 and PRMT5:MEP50 by ellagic acid could be used to develop breast cancer therapeutic drug.

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A Review on Picrosides Targeting NFκB and its Proteins for Treatment of Breast Cancer

Soni,

Anjum,

Raza

et al. 2024

Cell Biochem Biophys

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Dysregulation of different modes of programmed cell death by epigenetic modifications and their role in cancer

Cited by 4 publications

References 129 publications

Epigenetic regulation of diverse cell death modalities in cancer: a focus on pyroptosis, ferroptosis, cuproptosis, and disulfidptosis

Epigenetic regulation of diverse cell death modalities in cancer: a focus on pyroptosis, ferroptosis, cuproptosis, and disulfidptosis

Ellagic acid: a potential inhibitor of enhancer of zeste homolog-2 and protein arginine methyltransferase-5

A Review on Picrosides Targeting NFκB and its Proteins for Treatment of Breast Cancer

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