{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nRecent evidence indicates that the EP1 receptor (PTGER1) plays diverse and sometimes contrasting roles in cancer biology. In lung adenocarcinoma, EP1 mediates COX‐2–induced up‐regulation of VEGF‐C that promotes lymphangiogenesis, while in breast stromal cells, EP1 activation increases aromatase expression, thereby potentially influencing hormone‐dependent tumor growth. In oral cancer, EP1 activation contributes to enhanced migratory capacity and ICAM‐1 expression through PKCδ, Src and AP-1 signaling. Similarly, in hepatocellular carcinoma and cholangiocarcinoma models, EP1 signaling regulates cell adhesion and migration via modulation of integrin expression, FAK phosphorylation and MMP2 production. In non–small cell lung cancer, autocrine/paracrine PGE₂ signaling through EP1 has also been implicated in tumor progression, and studies in breast cancer have suggested that loss of nuclear EP1 may be associated with a poorer prognosis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its roles in tumor biology, EP1 is emerging as a critical modulator in neuroimmune and airway functions. In airway smooth muscle, although EP1 activation does not directly induce contraction, it forms heterodimers with β₂‐adrenergic receptors that diminish β₂–stimulated cAMP production and bronchodilation – a mechanism that may underlie β-agonist resistance in asthma. EP1 is also required for full activation of the hypothalamo-pituitary-adrenal axis after inflammatory stimuli and has been implicated in neuropathic pain pathways. Genetic association studies have linked PTGER1 polymorphisms with aspirin-intolerant asthma, while other investigations have revealed roles in dendritic cell development, myometrial contractility during labor, and even in central nervous system processes related to impulsive aggression and suicidal behavior."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "22"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAt the molecular level, EP1 receptor signaling demonstrates complex regulatory mechanisms. It is capable of physically associating with other receptors – for example, forming heterodimers with the dopamine D1 receptor to redirect coupling toward a specific adenylyl cyclase isoform (AC7), thereby modulating cAMP responses. EP1 also appears to function in a feedback loop that regulates inflammatory responses; increases in COX-2 expression can elevate EP1 levels, which in turn scaffold E3 ligases that promote COX-2 ubiquitination and proteasomal degradation. Beyond these signaling cascades, EP1 contributes to tissue differentiation and homeostasis – influencing keratinocyte differentiation in epidermis and modulating endometrial epithelial function in both normal and pathological states. Furthermore, EP1-mediated signaling can affect immune escape in colon cancer through regulation of Fas ligand expression, and combined EP receptor modulation has shown promise in enhancing bone healing in osteoblasts. These multifaceted roles underscore the potential of EP1 as both a prognostic marker and a therapeutic target in diverse pathophysiological conditions, including cardiovascular disease."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "23", "end_ref": "31"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jen-Liang Su, Jin-Yuan Shih, Men-Luh Yen, et al. 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