{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nProtein tyrosine kinase 7 (PTK7) is a catalytically defective receptor that plays vital roles in normal development by regulating planar cell polarity and non‐canonical Wnt signaling. Its unique gene organization sets it apart from conventional receptor tyrosine kinases and underpins its ability to interact with effectors such as β–catenin to modulate canonical Wnt responses and organizer formation. Moreover, PTK7 marks cells undergoing epithelial–mesenchymal transition during early embryoid body formation and its genetic disruption has been linked to neural tube defects, underscoring its importance in tissue organization and early morphogenesis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the oncology arena PTK7 is frequently deregulated and assumes context‐dependent roles that influence tumor cell survival, migration, invasion, and resistance to therapy. Elevated PTK7 expression has been observed in a broad range of malignancies—including prostate, colorectal, breast (notably triple–negative), esophageal, and lung adenocarcinomas—where its levels often correlate with aggressive behavior and poor clinical outcomes. In contrast, in certain lung squamous cell carcinomas ectopic PTK7 expression may inhibit proliferation and invasion, highlighting its dual functionality. Mechanistically, PTK7 activates key signaling cascades such as PI3K/Akt, ERK, and NF–κB and can modulate the activity of other cell–surface receptors (for example, by binding and activating fibroblast growth factor receptor 1 or influencing vascular endothelial growth factor receptor signaling). Furthermore, proteolytic processing by metalloproteinases (including ADAM17 and MT1–MMP) generates soluble extracellular fragments and intracellular domains that amplify its effects on cell motility and invasive capacity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "31"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its mechanistic roles in driving oncogenic signaling, PTK7 has emerged as a promising biomarker and therapeutic target. Advances in detection—such as the development of ultrasensitive aptasensor platforms based on bimetallic metal–organic frameworks—have enhanced the ability to monitor PTK7 expression in clinical samples. In addition, its regulation by noncoding RNAs (for example, suppression by miR–205 or modulation by the lncRNA MALAT1) reveals further complexity in its role in sustaining tumor cell proliferation, apoptosis resistance, and cell adhesion. Taken together, the multifaceted functions of PTK7 in both normal development and cancer underscore its potential as a diagnostic marker and as an actionable target for precision therapeutics."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "25"}, {"type": "fg_f", "ref": "32"}, {"type": "fg_f", "ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jae Won Jung, Ae Ri Ji, Jonghyeob Lee, et al. 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