Epigenetic mechanisms play a critical role in cancer progression, often acting together with genetic mutations to drive and stabilize the progressive changes observed as healthy cells undergo malignant transformation. All stages of cancer progression (malignant transformation, tumor growth, and metastasis) require the rewiring of a vast array of cellular functions, such as cell cycle control, cell plasticity, tissue invasion, cell migration, angiogenesis, immune system evasion, and inflammation. It is therefore not surprising that these gradual but significant changes in cell physiology are underpinned by the coordinated dysregulation of genome-wide gene expression programs.
Due to their ability to modulate the accessibility of a vast number of genomic loci, chromatin remodelers act as a gateway to regulating the transcription of a large repertoire of genes and indeed a growing body of evidence suggests that aberrant regulation of chromatin-modifying enzymes often fuel the emergence and maintenance of oncogenic phenotypes. In addition, recent evidence indicates that global alterations in the methylation status of regulatory DNA elements as well as of histone flags, i.e. post-translational modifications of histone tails, play an essential role in establishing oncogenic transcription programs. Furthermore, it has also been found that noncoding RNAs play an important role during cancer progression. Small noncoding RNAs, that target a large number of mRNAs based on sequence complementarity, have attracted a substantial amount of attention due to their ability to post-transcriptionally control and dysregulate gene expression. Although we are only beginning to fully appreciate the vast involvement of long non-coding RNAs (lncRNA) in a multitude of cellular mechanisms, recent evidence suggests that lncRNAs influence proliferation, survival, migration and cell plasticity, all of which contribute to the transformed phenotype of oncogenic cells.
The objective of this Research Topic is to review and discuss recent data and emerging concepts in the field of onco-epigenetics: we would like to shed light on the interplay of the dysregulation of gene expression and malignant transformation (tumor initiation) as well as the maintenance of the oncogenic phenotype (tumor growth, metastasis, angiogenesis, and immune system evasion). In particular, we would like to present different layers of epigenetic regulation (chromatin remodelers, histone marks, noncoding RNAs) as major drivers of the neoplastic process.
We welcome Original Research articles, Reviews, and Mini-Reviews focusing on:
1) The epigenetic changes (including chromatin remodeling, histone modifications, and noncoding RNAs) after cancer inducers, such as radiation or chemical compounds.
2) The study of how epigenetic changes contribute to cancer formation and progression, such as cell cycle control, cell plasticity, tissue invasion, cell migration, angiogenesis, immune system evasion, and inflammation.
3) Prognostic and Predictive biomarkers: identify epigenetic changes as new biomarkers for cancer diagnoses or treatments.
4) Advanced Technologies: the research of epigenetics and chromatin remodeling (e.g. 3D-mapping of the human genome by Hi-C technique and other new technologies for epigenetic study on cancer biology).
Epigenetic mechanisms play a critical role in cancer progression, often acting together with genetic mutations to drive and stabilize the progressive changes observed as healthy cells undergo malignant transformation. All stages of cancer progression (malignant transformation, tumor growth, and metastasis) require the rewiring of a vast array of cellular functions, such as cell cycle control, cell plasticity, tissue invasion, cell migration, angiogenesis, immune system evasion, and inflammation. It is therefore not surprising that these gradual but significant changes in cell physiology are underpinned by the coordinated dysregulation of genome-wide gene expression programs.
Due to their ability to modulate the accessibility of a vast number of genomic loci, chromatin remodelers act as a gateway to regulating the transcription of a large repertoire of genes and indeed a growing body of evidence suggests that aberrant regulation of chromatin-modifying enzymes often fuel the emergence and maintenance of oncogenic phenotypes. In addition, recent evidence indicates that global alterations in the methylation status of regulatory DNA elements as well as of histone flags, i.e. post-translational modifications of histone tails, play an essential role in establishing oncogenic transcription programs. Furthermore, it has also been found that noncoding RNAs play an important role during cancer progression. Small noncoding RNAs, that target a large number of mRNAs based on sequence complementarity, have attracted a substantial amount of attention due to their ability to post-transcriptionally control and dysregulate gene expression. Although we are only beginning to fully appreciate the vast involvement of long non-coding RNAs (lncRNA) in a multitude of cellular mechanisms, recent evidence suggests that lncRNAs influence proliferation, survival, migration and cell plasticity, all of which contribute to the transformed phenotype of oncogenic cells.
The objective of this Research Topic is to review and discuss recent data and emerging concepts in the field of onco-epigenetics: we would like to shed light on the interplay of the dysregulation of gene expression and malignant transformation (tumor initiation) as well as the maintenance of the oncogenic phenotype (tumor growth, metastasis, angiogenesis, and immune system evasion). In particular, we would like to present different layers of epigenetic regulation (chromatin remodelers, histone marks, noncoding RNAs) as major drivers of the neoplastic process.
We welcome Original Research articles, Reviews, and Mini-Reviews focusing on:
1) The epigenetic changes (including chromatin remodeling, histone modifications, and noncoding RNAs) after cancer inducers, such as radiation or chemical compounds.
2) The study of how epigenetic changes contribute to cancer formation and progression, such as cell cycle control, cell plasticity, tissue invasion, cell migration, angiogenesis, immune system evasion, and inflammation.
3) Prognostic and Predictive biomarkers: identify epigenetic changes as new biomarkers for cancer diagnoses or treatments.
4) Advanced Technologies: the research of epigenetics and chromatin remodeling (e.g. 3D-mapping of the human genome by Hi-C technique and other new technologies for epigenetic study on cancer biology).
