scholarly journals L-Ascorbic Acid in the Epigenetic Regulation of Cancer Development and Stem Cell Reprogramming

Acta Naturae ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 5-14
Author(s):  
A. P. Kovina ◽  
N. V. Petrova ◽  
S. V. Razin ◽  
O. L. Kantidze
Keyword(s):  
Ascorbic Acid ◽  
Stem Cell ◽  
Clinical Practice ◽  
Anticancer Therapy ◽  
Cancer Development ◽  
Cell Reprogramming ◽  
Active Demethylation ◽  
Somatic Cell Reprogramming ◽  
Epigenetic Drug ◽  
A Cell

Recent studies have significantly expanded our understanding of the mechanisms of L-ascorbic acid (ASC, vitamin C) action, leading to the emergence of several hypotheses that validate the possibility of using ASC in clinical practice. ASC may be considered an epigenetic drug capable of reducing aberrant DNA and histone hypermethylation, which could be helpful in the treatment of some cancers and neurodegenerative diseases. The clinical potency of ASC is also associated with regenerative medicine; in particular with the production of iPSCs. The effect of ASC on somatic cell reprogramming is most convincingly explained by a combined enhancement of the activity of the enzymes involved in the active demethylation of DNA and histones. This review describes how ASC can affect the epigenetic status of a cell and how it can be used in anticancer therapy and stem cell reprogramming.

scholarly journals Multiple Roles of p53-Related Pathways in Somatic Cell Reprogramming and Stem Cell Differentiation

2012 ◽  
Vol 72 (21) ◽  
pp. 5635-5645 ◽  
Author(s):  
Lan Yi ◽  
Chiwei Lu ◽  
Wenwei Hu ◽  
Yvonne Sun ◽  
Arnold J. Levine
Keyword(s):  
Stem Cell ◽  
Cell Differentiation ◽  
Somatic Cell ◽  
Stem Cell Differentiation ◽  
Multiple Roles ◽  
Cell Reprogramming ◽  
Somatic Cell Reprogramming

Ascorbic acid in epigenetic reprogramming

2021 ◽  
Vol 16 ◽  
Author(s):  
Xinhui Liu ◽  
Aamir Khan ◽  
Huan Li ◽  
Shensen Wang ◽  
Xuechai Chen ◽  
...  
Keyword(s):  
Ascorbic Acid ◽  
Vitamin C ◽  
Somatic Cell ◽  
Epigenetic Modification ◽  
Critical Role ◽  
Cellular Reprogramming ◽  
Epigenetic Reprogramming ◽  
Cell Reprogramming ◽  
Histone Demethylases ◽  
Somatic Cell Reprogramming

: Emerging evidence suggests that ascorbic acid (vitamin C) enhances the reprogramming process by multiple mechanisms. This is primarily due to its cofactor role in Fe(II) and 2-oxoglutarate-dependent dioxygenases, including the DNA demethylases Ten Eleven Translocase (TET) and histone demethylases. Epigenetic variations have been shown to play a critical role in somatic cell reprogramming. DNA methylation and histone methylation are extensively recognized as barriers to somatic cell reprogramming. N6-methyladenosine (m6A), known as RNA methylation, is an epigenetic modification of mRNAs and has also been shown to play a role in regulating cellular reprogramming. Multiple cofactors are reported to promote the activity of demethylases, including vitamin C. This review focuses on examining the evidence and mechanism of vitamin C in DNA and histone demethylation and highlights its potential involvement in regulating m6A demethylation. It also shows the significant contribution of vitamin C in epigenetic regulation and the affiliation of demethylases with vitamin C-facilitated epigenetic reprogramming.

scholarly journals Early epigenetic cancer decisions

2014 ◽  
Vol 395 (11) ◽  
pp. 1315-1320 ◽  
Author(s):  
Alberto Martín-Lorenzo ◽  
Inés Gonzalez-Herrero ◽  
Guillermo Rodríguez-Hernández ◽  
Idoia García-Ramírez ◽  
Carolina Vicente-Dueñas ◽  
...  
Keyword(s):  
Stem Cell ◽  
Target Cell ◽  
Current Model ◽  
Cellular Heterogeneity ◽  
Cancer Development ◽  
Cell Reprogramming ◽  
Anti Cancer ◽  
Developmental Reprogramming ◽  
Cancer Remission ◽  
Cancerous Cells

Abstract A cancer dogma states that inactivation of oncogene(s) can cause cancer remission, implying that oncogenes are the Achilles’ heel of cancers. This current model of cancer has kept oncogenes firmly in focus as therapeutic targets and is in agreement with the fact that in human cancers all cancerous cells, with independence of the cellular heterogeneity existing within the tumour, carry the same oncogenic genetic lesions. However, recent studies of the interactions between an oncogene and its target cell have shown that oncogenes contribute to cancer development via developmental reprogramming of the epigenome within the target cell. These results provide the first evidence that carcinogenesis can be initiated by epigenetic stem cell reprogramming, and uncover a new role for oncogenes in the origin of cancer. Here we analyse these evidences and discuss how this vision offers new avenues for developing novel anti-cancer interventions.

scholarly journals The THO Complex Regulates Pluripotency Gene mRNA Export and Controls Embryonic Stem Cell Self-Renewal and Somatic Cell Reprogramming

2013 ◽  
Vol 13 (6) ◽  
pp. 676-690 ◽  
Author(s):  
Li Wang ◽  
Yi-Liang Miao ◽  
Xiaofeng Zheng ◽  
Brad Lackford ◽  
Bingying Zhou ◽  
...  
Keyword(s):  
Stem Cell ◽  
Embryonic Stem Cell ◽  
Somatic Cell ◽  
Mrna Export ◽  
Embryonic Stem ◽  
Cell Reprogramming ◽  
Self Renewal ◽  
Somatic Cell Reprogramming ◽  
Pluripotency Gene ◽  
Gene Mrna

scholarly journals Impaired stem cell differentiation and somatic cell reprogramming in DIDO3 mutants with altered RNA processing and increased R-loop levels

2021 ◽  
Vol 12 (7) ◽  
Author(s):  
Agnes Fütterer ◽  
Amaia Talavera-Gutiérrez ◽  
Tirso Pons ◽  
Jesús de Celis ◽  
Julio Gutiérrez ◽  
...  
Keyword(s):  
Stem Cell ◽  
Somatic Cell ◽  
Rna Processing ◽  
Transcription Termination ◽  
Regulation Of Gene Expression ◽  
Embryonic Stem ◽  
Stem Cell Differentiation ◽  
Cell Reprogramming ◽  
Main Role ◽  
Somatic Cell Reprogramming

AbstractEmbryonic stem cell (ESC) differentiation and somatic cell reprogramming are biological processes governed by antagonistic expression or repression of a largely common set of genes. Accurate regulation of gene expression is thus essential for both processes, and alterations in RNA processing are predicted to negatively affect both. We show that truncation of the DIDO gene alters RNA splicing and transcription termination in ESC and mouse embryo fibroblasts (MEF), which affects genes involved in both differentiation and reprogramming. We combined transcriptomic, protein interaction, and cellular studies to identify the underlying molecular mechanism. We found that DIDO3 interacts with the helicase DHX9, which is involved in R-loop processing and transcription termination, and that DIDO3-exon16 deletion increases nuclear R-loop content and causes DNA replication stress. Overall, these defects result in failure of ESC to differentiate and of MEF to be reprogrammed. MEF immortalization restored impaired reprogramming capacity. We conclude that DIDO3 has essential functions in ESC differentiation and somatic cell reprogramming by supporting accurate RNA metabolism, with its exon16-encoded domain playing the main role.

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