{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSMARCA4, also known as BRG1, is a pivotal ATPase subunit of the SWI/SNF chromatin‐remodeling complex that orchestrates dynamic nucleosomal reorganization and regulates gene expression in diverse biological settings. Its downregulation by macrophage‐derived microRNAs has been shown to promote colorectal cancer cell migration and invasion, underscoring its importance in controlling metastatic behavior."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " In the developing heart, SMARCA4 regulates cardiomyocyte proliferation and directs the fetal‐to‐adult myosin heavy chain switch – a process that becomes reactivated under cardiac stress, contributing to pathological hypertrophy."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": " By interacting with the transcription factor ZEB1, SMARCA4 plays a key role in repressing E‐cadherin expression to promote epithelial‐to‐mesenchymal transition (EMT) during tumor invasion"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": ", while its participation in complexes with p53 supports its function in cell‐cycle control and tumor suppression"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": "and."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": " Moreover, SMARCA4 is required for glucocorticoid receptor–mediated trans‐repression of proopiomelanocortin and for facilitating Nrf2‐dependent induction of antioxidant genes"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": "and"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": ", and it localizes to critical enhancer elements in hematopoietic cells to shape cell‐type–specific transcriptional programs."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": " Its mechanistic role is further underscored by studies demonstrating that SMARCA4 mutants disrupt enhancer accessibility and nucleosome remodeling dynamics"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "9"}]}, {"type": "t", "text": "and"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "10"}]}, {"type": "t", "text": ", while its participation in signal‐dependent pathways is evident from its interaction with SMAD transcription factors during TGF‑β signaling."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn oncogenesis, inactivating mutations and loss of SMARCA4 expression have emerged as critical events in several aggressive malignancies. Germline mutations in SMARCA4 predispose to small cell carcinoma of the ovary, hypercalcemic type (SCCOHT)"}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "15"}]}, {"type": "t", "text": ", and"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "16"}]}, {"type": "t", "text": ", while its loss in non‐small cell lung cancers correlates with adverse outcomes"}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "17", "end_ref": "27"}]}, {"type": "t", "text": ", and."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "28"}]}, {"type": "t", "text": " In these contexts, defective SMARCA4 impairs chromatin remodeling processes that maintain genomic stability and proper cell cycle checkpoints, thereby facilitating malignant transformation, enhanced invasiveness, and dedifferentiation. Notably, such loss of function disrupts tumor‐suppressive networks and cellular adhesion that normally restrain metastatic progression (for example, via perturbation of p53‐mediated regulation and altered chromatin states)."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nEmerging evidence has further revealed that SMARCA4 deficiency creates exploitable therapeutic vulnerabilities. Synthetic‐lethal approaches targeting its paralog SMARCA2, as well as the use of EZH2 and oxidative phosphorylation inhibitors, show promise in preclinical models"}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "30", "end_ref": "33"}]}, {"type": "t", "text": ", and."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "34"}]}, {"type": "t", "text": " Restoration of SMARCA4 function reengages transcriptional circuits controlling cell differentiation, as evidenced by its role in configuring enhancer landscapes in both hematopoietic and melanocytic lineages"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "35"}]}, {"type": "t", "text": "and."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "36"}]}, {"type": "t", "text": " Moreover, aberrant enhancer reprogramming linked to SMARCA4 loss has been implicated in further modulation of lineage‐determining transcriptional networks (for instance, through altered chromatin interactions affecting global gene expression patterns ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "37"}]}, {"type": "t", "text": "]), while its regulatory influence over differentiation is also observed in melanocytes and other cell types"}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "38", "end_ref": "40"}]}, {"type": "t", "text": ", and."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "41"}]}, {"type": "t", "text": " Finally, aberrant chromatin remodeling by SMARCA4 also impacts vascular smooth muscle cell function, contributing to epigenetic repression of contractile gene expression and the pathogenesis of aortic aneurysms."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "42"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jingqin Lan, Li Sun, Feng Xu, et al. 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