{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nRSF1 is frequently amplified and overexpressed in a variety of human malignancies—including ovarian, oral, colon, nasopharyngeal, lung, breast, and hepatocellular carcinomas—and its elevated expression correlates with aggressive tumor behavior and poor clinical outcomes. In ovarian and other high‐grade serous carcinomas, RSF1 amplification is associated with increased cell proliferation, transformation, chemoresistance (for example, paclitaxel resistance), and shorter overall survival. Similar correlations between RSF1 overexpression and advanced tumor stage, metastasis, and reduced patient survival have been documented in studies of oral squamous cell, colon, urothelial, and breast cancers, as well as in analyses linking RSF1 levels with immune‐related susceptibility in infectious disease cohorts."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAs a critical chromatin remodeling factor, RSF1 functions primarily through forming a complex with hSNF2H (also known as SNF2H) to orchestrate nucleosome organization and regulate gene expression. RSF1 facilitates cell cycle progression by modulating key regulators such as cyclin E1 and phospho‐Rb, and it exerts transcriptional control by acting as a reader for histone H2A ubiquitination marks that are linked to gene silencing. Moreover, RSF1 plays an essential role in the DNA damage response by promoting both homologous recombination and non‐homologous end joining repair, recruiting factors like XRCC4, and engaging with checkpoint pathways—including p53‐dependent signaling—that help maintain genomic integrity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "20"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in chromatin remodeling and DNA repair, RSF1 contributes to the faithful progression of mitosis by recruiting key mitotic kinases. It promotes proper chromosome alignment and segregation through the targeting of PLK1 to kinetochores and subsequent activation of Aurora B. RSF1 also collaborates with histone deacetylases (for example, recruiting HDAC1) to modify local chromatin structure at double‐strand break sites—thereby coupling transcriptional repression with efficient repair—and is itself subject to regulation by noncoding RNAs. Tumor‐suppressive microRNAs (such as miR‑154 and miR‑129‑5p) and long noncoding RNAs (for example, SNHG6) have been shown to target RSF1, while RSF1 activity can modulate NF‑κB signaling and promote chemoresistance in certain settings. In addition, emerging evidence implicates RSF1 or its circular RNA derivative in modulating the inflammatory phenotype in non‑tumor contexts, further highlighting its multifaceted regulatory roles."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "21", "end_ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Ie-Ming Shih, Jim Jinn-Chyuan Sheu, Antonio Santillan, et al. 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