Special Issue "Transcription and Chromatin Dysregulation in Cancer"
Deadline for manuscript submissions: closed (20 June 2023) | Viewed by 5227
Interests: cancer epigenomics; RNA biology; cancer cell signaling; gene regulation
Interests: cancer genetics; epigenetics; RNA biology; RNA–protein interaction; RNA therapeutics; post-translational modification; non-coding RNAs; stress biology
Cellular homeostasis relies on the programmed transcriptional machinery in a cell. Any disruption in the process of transcriptional control in turn causes aberrant gene expression that underscores the main hallmarks of cancer cells. Generally, the molecular regulators of these programmed signaling cascades involve transcription factors (TFs), which are being extensively studied to be targeted by various anti-tumor therapeutic approaches. However, recent advances in sequencing the data of cancer genomes have unveiled several changes occurring at the level of chromatin structure and epigenetics, affecting other components of the transcriptional control involving cis and trans regulatory elements and chromatin modifiers. Hence, it is of the utmost importance to understand how chromatin modifiers integrate both extracellular and cytoplasmic signals to control gene activity. Most common dysregulation occurring at the level of chromatin remodelers leading to oncogenesis involves inactivating mutations in SWI/SNF complex, epigenetic silencing via DNA and histone hypermethylation, and overexpression of oncogenic chromatin modifiers (Mi-2/NuRD proteins). In addition, the pattern of histone modification also controls the tumorigenic nature of cells depending on interaction between TFs and histone modifiers. One such modification involves the monomethylation of histone H3 at lysine 4 (H3K4me1) and acetylation at lysine 27 (H3K27ac), leading to the activation of a long stretch of oncogenic enhancers called super-enhancers (SEs).
The aim of this Special Issue is to explore and provide our readers with more insight into the oncogenic signal(s) and regulatory mechanisms at the level of chromatin that drive cancer development and progression. We invite original communications and review articles which can help us to understand the complex nature of epigenetic regulation that transforms the canonical role of TFs to become oncogenic, and how the interaction dynamics between chromatin modifiers, histone marks and cis/trans regulatory elements controls the entire tumorigenic landscape, with a view to identifying probable new cancer biomarkers and strategies for targeting them as means of therapeutic intervention.
Dr. Yinghui Li
Dr. Kamalakshi Deka
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- transcriptional regulation
- chromatin modifiers
- chromatin dysregulation
- chromatin interaction
- histone modification
- cancer cell signaling