TL;DR
The role of nuclear architecture in tumorigenesis, the contribution of lamins to chromatin organization, and the emerging epigenetic control of lamins in cancer progression and metastasis are discussed.
A comprehensive synthesis of the mechanisms and functional roles of classical chromatin remodelers within both physiological and neoplastic contexts is provided and a hierarchical framework that distinguishes between 'first-level' and 'higher-order' chromatin remodeling is proposed.
A unified view is provided of how genome structure is established, how it relates to function, and how its disruption contributes to tumorigenesis, suggesting that alterations in genome structure can, in some contexts, actively reshape oncogenic programs.
A unified mechanistic framework by which the level of YAP/TAZ activity determines enhancer landscapes that favor either differentiated or progenitor-like cellular states is proposed, providing a potential basis for applications to regenerative medicine and therapeutic interventions.
Dysregulation of three-dimensional (3D) genome architecture is a hallmark of cancer, yet the mechanisms by which its disruption drives tumorigenesis remain incompletely understood. Here, we demonstrated that SMAD4 regulated 3D genome organization through its canonical transcription factor activity by directly binding c...
The unique 3D chromatin variation pattern in cancers may become a new biomarker and provide a theoretical basis for epigenetic therapy targeting chromatin spatial organization.
The role of the critical nuclear speckle component SON was examined and it was shown that it is required for myofibroblast gene expression and support a model in which distinct facets of genome organization converge to orchestrate cell-state transitions.
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