{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nPRRX1 is a homeobox transcription factor that plays a pivotal role in orchestrating epithelial–mesenchymal transition (EMT) and regulating cancer cell plasticity. In several solid malignancies—including breast, thyroid, colorectal, gastric, pancreatic, glioblastoma, and hepatocellular carcinoma—PRRX1 acts as an EMT inducer that confers migratory and invasive capacities on tumor cells. In many instances, its high expression promotes dedifferentiation and invasion, whereas its subsequent downregulation can trigger a mesenchymal–epithelial transition (MET) associated with the re‐acquisition of epithelial features and cancer stem cell properties necessary for metastatic colonization. Moreover, isoform‐specific roles have been described; for example, one splice variant may enhance EMT and dissemination, while another facilitates metastatic outgrowth. These multifaceted functions are linked to PRRX1’s ability to modulate key signaling pathways—including TGF‑β, Wnt/β‑catenin, and Notch—which together govern cell adhesion, stemness, and even therapeutic resistance."}, {"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": "\nAdditional layers of regulation further refine PRRX1’s impact in cancer. Its expression and activity are subject to modulation by noncoding RNAs and interacting transcriptional partners. For instance, microRNAs (such as miR‑1307) directly target PRRX1, while circular RNAs derived from the PRRX1 locus (exosomal circPRRX1) have been implicated in altering cellular responses to chemotherapy and ionizing radiation. Interactions with factors like FOXM1 not only influence PRRX1‑dependent gene regulation but also affect downstream signaling via pathways such as PTEN/PI3K/AKT. These regulatory circuits contribute to multidrug resistance, altered cell survival, and perturbed tumor cell differentiation, suggesting that the PRRX1 regulatory axis may offer promising therapeutic targets."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "15", "end_ref": "23"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond cancer, PRRX1 is critical in various developmental and nonneoplastic contexts. Mutations and altered expression of PRRX1 have been associated with congenital malformations such as agnathia–otocephaly and craniosynostosis, while genetic variants predispose to conditions like atrial fibrillation. In addition, PRRX1 regulates cellular quiescence in neural progenitors and oligodendrocyte precursor cells, and modulates extracellular matrix production in hepatic stellate cells and adipose tissue—a function relevant to fibrosis and metabolic dysfunction. Rearrangements involving PRRX1 have also been characterized in rare fibroblastic tumors, underscoring its broader role in tissue development and homeostasis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "24", "end_ref": "33"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Oscar H Ocaña, Rebeca Córcoles, Angels Fabra, et al. 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