Epigenetic control of programmed cell death: inhibition by 5-azacytidine of 1,25-dihydroxyvitamin D3-induced programmed cell death in C6.9 glioma cells

Canova, Cécile; Chevalier, G.; Remy, Séverine; Brachet, Philippe; Wion, Didier

doi:10.1016/s0047-6374(97)00172-3

Cited by 12 publications

(5 citation statements)

References 57 publications

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“…Recent studies have indicated that epigenetic modifications were involved in the PCD process . To study the exact relationship between PCD and epigenetic modifications, we selected the TNF‐α and CHX‐induced apoptosis process in the murine cell line NIH‐3T3 as a model.…”

Section: Resultsmentioning

confidence: 99%

“…Recent studies have indicated that epigenetic modifications were involved in the PCD process. 33 To study the exact relationship between PCD and epigenetic modifications, we selected the TNF-α and CHX-induced apoptosis process in the murine cell line NIH-3T3 as a model. Treatment of NIH-3T3 cells with 30 ng/ml TNF-α and 30 µg/ml CHX for 8 h showed that apoptosis cells significantly increased as compared with the untreated cells and the apoptotic rate was approximately 40% (Figure 1A).…”

Section: The Tnf-α and Chx-induced Apoptosis Process In The Murine Ce...mentioning

confidence: 99%

“…Recently, it has been reported that DNA methylation inhibitors coordinating with BCL‐2 family inhibitors sensitizes cancer cells to apoptosis more efficiently than single agent . Contrastingly, Canova et al reported that 5‐AC epigenetically inhibited the 1,25‐dihydroxyvitamin D3‐induced apoptosis in C6.9 Glioma cells . Whether DNA methylation is one of the regulators in PCD and the underlying mechanism in apoptosis is yet required to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

“…[29][30][31][32] Contrastingly, Canova et al reported that 5-AC epigenetically inhibited the 1,25-dihydroxyvitamin D3-induced apoptosis in C6.9 Glioma cells. 33 Whether DNA methylation is one of the regulators in PCD and the underlying mechanism in apoptosis is yet required to be elucidated. Tumor necrosis factor alpha (TNF-α) could induce apoptosis and cycloheximide (CHX), which is a protein synthesis inhibitor, could enhance this apoptosis process.…”

Section: Introductionmentioning

confidence: 99%

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5‐Azacytidine specifically inhibits the NIH‐3T3 PCD process induced by TNF‐alpha and cycloheximide via affecting BCL‐XL

Wang

Zhou

et al. 2017

J of Cellular Biochemistry

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DNA methylation plays a crucial role in lots of biological processes and cancer. 5-azacytidine (5-AC), a DNA methylation inhibitor, has been used as a potential chemotherapeutic agent for cancer. In this study, we used 5-AC treatment to investigate whether DNA methylation was involved in regulation of programmed cell death (PCD) in mouse embryo fibroblast NIH-3T3 cells which could undergo PCD after treatment with TNF-α and cycloheximide (CHX). The results showed that the genomic DNA of NIH-3T3 cells was hypermethylated during PCD induced by TNF-α and CHX, and 5-AC might prevent this PCD process. However, treatment with the other three DNA methylation inhibitors, 5-aza-deoxycytidine, 6-thioguanine and RG108, did not interfere with the NIH-3T3 cell PCD process. Additionally, knockdown of DNMT1 did not affect the apoptosis process. The present results and observations indicated that 5-AC specifically inhibited the NIH-3T3 apoptosis process via a genomic DNA methylation-independent pathway. During the TNF-α and CHX-inducing apoptosis process, the PCD related BCL-2 family proteins were significantly down-regulated. Furthermore, after the small interference RNA-mediated knockdown of BCL-XL, one of the BCL-2 family proteins, 5-AC did not inhibit the apoptosis process, suggesting that 5-AC inhibited the PCD process induced by TNF-α and CHX by affecting the anti-apoptotic protein BCL-XL.

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Section: Resultsmentioning

confidence: 99%

Section: The Tnf-α and Chx-induced Apoptosis Process In The Murine Ce...mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

5‐Azacytidine specifically inhibits the NIH‐3T3 PCD process induced by TNF‐alpha and cycloheximide via affecting BCL‐XL

Wang

Zhou

et al. 2017

J of Cellular Biochemistry

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“…These findings suggest that the efficiency of antiproliferative vitamin D-related therapies could be influenced by endogenous levels of noradrenaline (32). Furthermore, changes in the DNA methylation pattern could suppress 1,25(OH) 2 D 3 -mediated apoptosis via expression of hypermethylated genes, such as proto- oncogenes, with death-repressor activity (33). …”

Section: Vitaminsmentioning

confidence: 99%

Modulation of Glioma Risk and Progression by Dietary Nutrients and Antiinflammatory Agents

2011

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Gliomas are tumors of glial origin formed in the central nervous system and exhibit profound morphological and genetic heterogeneity. The etiology of this heterogeneity involves an interaction between genetic alterations and environmental risk factors. Scientific evidence suggests that certain natural dietary components, such as phytoestrogens, flavonoids, polyunsaturated fatty acids and vitamins may exert a protective effect against gliomas by changing the nature of the interaction between genetics and environment. Similarly, certain anti-inflammatory drugs and dietary modifications, such as methionine restriction and the adoption of low-calorie or ketogenic diets, may take advantage of glioma and normal glial cells’ differential requirements for glucose, methionine, and ketone bodies and may therefore be effective as part of preventive or treatment strategies for gliomas. Treatment trials of glioma patients and chemoprevention trials of individuals with a known genetic predisposition to glioma using the most promising of these agents, such as the anti-inflammatory drugs curcumin and gamma-linolenic acid, are needed to validate or refute these agents’ putative role in gliomas.

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From epidemiology and neurometabolism to treatment: Vitamin D in pathogenesis of glioblastoma Multiforme (GBM) and a proposal for Vitamin D + all-trans retinoic acid + Temozolomide combination in treatment of GBM

et al. 2019

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Epigenetic control of programmed cell death: inhibition by 5-azacytidine of 1,25-dihydroxyvitamin D3-induced programmed cell death in C6.9 glioma cells

Cited by 12 publications

References 57 publications

5‐Azacytidine specifically inhibits the NIH‐3T3 PCD process induced by TNF‐alpha and cycloheximide via affecting BCL‐XL

5‐Azacytidine specifically inhibits the NIH‐3T3 PCD process induced by TNF‐alpha and cycloheximide via affecting BCL‐XL

Modulation of Glioma Risk and Progression by Dietary Nutrients and Antiinflammatory Agents

From epidemiology and neurometabolism to treatment: Vitamin D in pathogenesis of glioblastoma Multiforme (GBM) and a proposal for Vitamin D + all-trans retinoic acid + Temozolomide combination in treatment of GBM

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