{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nPTTG1, originally identified as the pituitary tumor‐transforming gene and the human securin, has emerged as a multifunctional protein whose deregulation is linked not only to genetic susceptibility in conditions such as psoriasis but also to a wide range of human neoplasms. In normal physiology, PTTG1 plays a crucial role in cell cycle control by regulating sister chromatid cohesion and separation during mitosis, ensuring genomic stability. Genetic association studies and candidate gene analyses have also implicated PTTG1 as one of several susceptibility factors in complex diseases, underscoring its broader biological significance."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "9"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMechanistically, PTTG1 functions as the securin protein that binds to and inhibits separase, thereby preventing premature cleavage of cohesin complexes during metaphase–anaphase transition. Its timely degradation is essential for accurate chromatid separation, and failures in this process can lead to aneuploidy and chromosomal instability—a common feature in many cancers. In addition to its classical cell cycle role, PTTG1 also acts as a transcriptional modulator; it interacts with key molecules such as p53 to inhibit DNA binding and transcriptional activities involved in apoptosis and growth arrest. Elevated PTTG1 expression has been correlated with aggressive tumor traits, recurrence and poor prognosis in several endocrine and nonendocrine malignancies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "10", "end_ref": "19"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in cell cycle regulation and transcriptional control, PTTG1 acts as a potent oncogenic driver by promoting angiogenesis, epithelial-to-mesenchymal transition (EMT), and cell invasion. It stimulates the expression of growth factors such as FGF‐2 and VEGF, and activates multiple signaling cascades including beta‐catenin/WNT, integrin–FAK, and Akt pathways that are integral to cytoskeletal remodeling, motility, and metastatic progression. Moreover, modulation of its expression by microRNAs and activation by transcription factors such as STAT3 and c‐Myc further fine‐tune its function in tumorigenesis. Consequently, PTTG1 overexpression has been associated with enhanced tumor cell migration, invasion, and metastasis in cancers of the breast, lung, thyroid, esophagus, kidney, and brain, marking it as a promising prognostic biomarker and therapeutic target."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "20", "end_ref": "40"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Liang-Dan Sun, Hui Cheng, Zai-Xing Wang, et al. 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