Epigenetic regulation generally implicates the dynamic modifications of the histones, the DNA, and RNA, though can conversely also involve maintaining the silencing of specific genes. The epigenetic modulators (i.e. 'writers', 'readers' and 'erasers') can render “on-off” switches by modifying the substrates, and therefore set up a unique nuclear environment for executing the molecular actions of chromatin. Transcription factors typically bind to the chromatin via cognate DNA motifs, and involve complex molecular machinery to drive gene transcription. Transcriptional reprogramming is a common determinant for how cancer cells develop drug resistance, and also in how they metastasize to secondary sites. Recent sequencing research in patients has revealed that mutations are commonly found in both epigenetic and transcriptional machinery in the nuclear environment, highlighting the importance of understanding the molecular functions of both of these factors in tandem, rather than in isolation.
The acquired oncogenic transcription programs require the pertinent chromatin stage, which can be set up by the epigenetic modifiers. How epigenetic modulators cooperate with transcription complexes in order to regulate the oncogenic program still remains largely unknown and requires further research. In particular, transcription factors are typically non-druggable, due to the lack of a targetable domain. On the other hand, there has been a rapid development of small molecules targeting various players in epigenetic modification. More importantly, recent research has illuminated multiple novel functions of epigenetic modifiers playing a regulatory role in RNA splicing, such as novel substrates in the nuclear environment. Therefore identifying the crosstalk between epigenetic and transcriptomic factors may provide researchers with important insights enabling the identification of new therapeutic targets, and to subsequently develop novel therapeutic approaches. This can be achieved by utilizing multi-omic based tools which incorporate biochemical, structural, and imaging analyses.
In this research topic, we welcome submissions of Original Research and leading-edge reviews, which include but are not limited to, the following themes:
1. Regulation of chromatin-associated factors in chromosomal rearrangements and gene transcription during drug resistance and metastasis;
2. The impact of external stimuli on the nuclear environment;
3. The biological functions of genetic alterations on the chromatin-associated factors;
4. Understand the molecular crosstalk between epigenetic and transcription modulators;
5. Identify novel therapies to overcome drug resistance.
Please note: manuscripts that are solely based on bioinformatics or computational analysis of public databases without validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
Epigenetic regulation generally implicates the dynamic modifications of the histones, the DNA, and RNA, though can conversely also involve maintaining the silencing of specific genes. The epigenetic modulators (i.e. 'writers', 'readers' and 'erasers') can render “on-off” switches by modifying the substrates, and therefore set up a unique nuclear environment for executing the molecular actions of chromatin. Transcription factors typically bind to the chromatin via cognate DNA motifs, and involve complex molecular machinery to drive gene transcription. Transcriptional reprogramming is a common determinant for how cancer cells develop drug resistance, and also in how they metastasize to secondary sites. Recent sequencing research in patients has revealed that mutations are commonly found in both epigenetic and transcriptional machinery in the nuclear environment, highlighting the importance of understanding the molecular functions of both of these factors in tandem, rather than in isolation.
The acquired oncogenic transcription programs require the pertinent chromatin stage, which can be set up by the epigenetic modifiers. How epigenetic modulators cooperate with transcription complexes in order to regulate the oncogenic program still remains largely unknown and requires further research. In particular, transcription factors are typically non-druggable, due to the lack of a targetable domain. On the other hand, there has been a rapid development of small molecules targeting various players in epigenetic modification. More importantly, recent research has illuminated multiple novel functions of epigenetic modifiers playing a regulatory role in RNA splicing, such as novel substrates in the nuclear environment. Therefore identifying the crosstalk between epigenetic and transcriptomic factors may provide researchers with important insights enabling the identification of new therapeutic targets, and to subsequently develop novel therapeutic approaches. This can be achieved by utilizing multi-omic based tools which incorporate biochemical, structural, and imaging analyses.
In this research topic, we welcome submissions of Original Research and leading-edge reviews, which include but are not limited to, the following themes:
1. Regulation of chromatin-associated factors in chromosomal rearrangements and gene transcription during drug resistance and metastasis;
2. The impact of external stimuli on the nuclear environment;
3. The biological functions of genetic alterations on the chromatin-associated factors;
4. Understand the molecular crosstalk between epigenetic and transcription modulators;
5. Identify novel therapies to overcome drug resistance.
Please note: manuscripts that are solely based on bioinformatics or computational analysis of public databases without validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
