Chromatin Remodeling Complexes in Tumor Progression: From SWI/SNFDysfunction to Precision Oncology
Keywords:
Chromatin remodeling; SWI/SNF complex; epigenetics; tumor progression; precision oncologyAbstract
Chromatin remodeling complexes are fundamental regulators of genome
accessibility, transcriptional plasticity, DNA repair, and epigenetic
homeostasis. Among these, the SWI/SNF (Switch/Sucrose Non-
Fermentable) family has emerged as one of the most frequently altered
chromatin remodeling systems in human malignancies. Accumulating
evidence demonstrates that mutations, deletions, and epigenetic
dysregulation of SWI/SNF subunits contribute substantially to tumor
initiation, progression, metastatic dissemination, and therapeutic
resistance. Dysfunction of key components including ARID1A,
SMARCB1, SMARCA4, and PBRM1 reshapes chromatin architecture,
perturbs enhancer activity, and promotes oncogenic transcriptional
programs across diverse cancer types. Recent advances in next-generation
sequencing, epigenomic profiling, and precision oncology have further
elucidated the intricate interplay between chromatin remodeling defects
and tumor microenvironment dynamics, immune evasion, and lineage
plasticity. Importantly, the therapeutic vulnerability associated with
SWI/SNF deficiency has stimulated the development of targeted
interventions, including EZH2 inhibitors, bromodomain inhibitors,
synthetic lethality-based approaches, and immunotherapeutic strategies.
This review provides an overview of the molecular architecture of
chromatin remodeling complexes, with particular emphasis on SWI/SNF
dysfunction in cancer biology and its emerging translational relevance in
precision oncology.
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