Abstract
Disordered 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.
Highlights
Normal gene transcription is fundamental for cell physiology
Chromatin remodeling complexes (CRCs) are multisubunit transcription complexes (TCs) containing a series of ATP-dependent remodeling enzymes, which act as ‘molecular motors’ that couple ATP hydrolysis to the perturbation of histone-DNA contacts with respect to individual nucleosome core particles [1]
Through TCGA database analysis, we found that BAZ1A, CHRAC1 and POLE3 are simultaneously upregulated in a variety of tumors, such as esophageal carcinoma (ESCA), liver hepatocellular carcinoma (LIHC), stomach adenocarcinoma (STAD), breast invasive carcinoma (BRCA), etc. (Fig. 2A)
Summary
Normal gene transcription is fundamental for cell physiology. The gene transcription program is executed by transcription complexes (TCs). Chromatin remodeling complexes (CRCs) are multisubunit TCs containing a series of ATP-dependent remodeling enzymes, which act as ‘molecular motors’ that couple ATP hydrolysis to the perturbation of histone-DNA contacts with respect to individual nucleosome core particles [1]. Based on the sequence homology of the catalytic ATPase and the accessory subunits, CRCs are divided into four main. A growing number of preclinical and clinical studies have highlighted that ISWI complexes play critical pathological roles in tumorigenesis, tumor development, tumor immunity and drug response. ISWI subunits display multiple functions in affecting tumor cell phenotypes via regulation of oncogenic gene transcription. Copy number changes or translocations have been identified that may produce gain/
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