{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nTRPS1, an atypical GATA-family transcription factor, plays a critical role in breast cancer pathobiology by modulating epithelial‐to‐mesenchymal transition (EMT) and serving as a robust diagnostic marker. In basal‐like breast tumors, for example, microRNAs such as miR‐221/222 target the 3′UTR of TRPS1 to decrease epithelial markers and promote mesenchymal attributes, thereby enhancing cell invasion and migration. Complementary studies have demonstrated that TRPS1 is overexpressed across multiple breast cancer subtypes—including ER‐positive, HER2‐positive, and triple‐negative forms—and that its detection outperforms other markers in certain diagnostic contexts. Its expression in both in situ and invasive lesions further underscores a role in ductal epithelial cell differentiation and, in some settings, correlates with improved clinical outcome."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "14"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAt the molecular level, TRPS1 orchestrates diverse transcriptional programs by acting as both a repressor and, under select circumstances, an activator. It directly binds regulatory regions of key target genes—for instance, repressing EMT drivers such as ZEB2 while activating factors like FOXA1—to control cell state and proliferation. TRPS1 engages with several corepressor complexes (including NuRD and coREST) and undergoes post‐translational modifications (such as SUMOylation) that fine‐tune its repressor activity. In addition, interactions with nuclear partners such as RNF4, BAT3, and even the Hippo pathway effector YAP further modulate its capacity to control enhancer acetylation and gene expression networks. These mechanistic insights in breast cancer models suggest that through coordinated transcriptional repression, TRPS1 not only influences EMT and cell cycle progression but also shapes the tumor’s immune and proliferative microenvironments."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "15", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its oncogenic and diagnostic significance in breast cancer, TRPS1 is integral to broader developmental and tumor biological processes. It is a key regulator of bone, hair, and tooth morphogenesis—as evidenced by its mutated or deleted alleles in tricho‐rhino‐phalangeal syndromes—and modulates cell cycle checkpoints, mitotic progression, and apoptosis. In varied malignancies such as lung, osteosarcoma, and prostate cancer, aberrant TRPS1 expression impacts chemoresistance by influencing drug efflux and DNA repair gene transcription (e.g. via regulation of MDR1/P‐gp and MGMT). These multifaceted functions position TRPS1 as a complex, context‐dependent mediator that not only governs differentiation and mineralization but also contributes to tumor initiation, progression, and therapeutic response."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "29", "end_ref": "41"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Susanna Stinson, Mark R Lackner, Alex T Adai, et al. 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