Author:
Li Yanan,Gong Han,Wang Pan,Zhu Yu,Peng Hongling,Cui Yajuan,Li Heng,Liu Jing,Wang Zi
Abstract
AbstractDisordered chromatin remodeling regulation has emerged as an essential driving factor for cancers. Imitation switch (ISWI) family are evolutionarily conserved ATP-dependent chromatin remodeling complexes, which are essential for cellular survival and function through multiple genetic and epigenetic mechanisms. Omics sequencing and a growing number of basic and clinical studies found that ISWI family members displayed widespread gene expression and genetic status abnormalities in human cancer. Their aberrant expression is closely linked to patient outcome and drug response. Functional or componential alteration in ISWI-containing complexes is critical for tumor initiation and development. Furthermore, ISWI-non-coding RNA regulatory networks and some non-coding RNAs derived from exons of ISWI member genes play important roles in tumor progression. Therefore, unveiling the transcriptional regulation mechanism underlying ISWI family sparked a booming interest in finding ISWI-based therapies in cancer. This review aims at describing the current state-of-the-art in the role of ISWI subunits and complexes in tumorigenesis, tumor progression, immunity and drug response, and presenting deep insight into the physiological and pathological implications of the ISWI transcription machinery in cancers.
Funder
national key research and development program of china
national natural science foundation of china
national postdoctoral program for innovative talents
natural science foundation of hunan province
science and technology key project of hunan province
the fundamental research funds for the central universities of central south university
Publisher
Springer Science and Business Media LLC
Cited by
26 articles.
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