{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nStudies in non‐small cell lung cancer have shown that overexpression of miR-337–3p enhances the sensitivity of cancer cells to taxane chemotherapies by directly targeting key mediators such as STAT3 and RAP1A. This effect suggests that miR-337–3p may be harnessed as an adjuvant to overcome chemoresistance."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn epithelial ovarian cancer, miR-337–3p is frequently downregulated, and restoration of its levels inhibits cell proliferation and induces apoptosis and cell cycle arrest by targeting the catalytic subunits PIK3CA and PIK3CB, thereby dampening PI3K/AKT signaling. Moreover, in gastric cancer and neuroblastoma, miR-337–3p directly represses transcription of matrix metalloproteinase genes (for example, MMP-14) and cytoskeleton-associated signaling molecules like ARHGAP10, which contributes to the inhibition of cell invasion, metastasis, and angiogenesis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "2", "end_ref": "4"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn cervical cancer, multiple reports indicate that miR-337 (including the –3p isoform) acts as a tumor suppressor. Its ectopic expression can inhibit cell proliferation, migration, and invasion by targeting genes such as specificity protein 1 and Rap1A, while loss of miR-337 activity—often mediated by sponging effects of circular RNAs like circ_0000388—leads to enhanced malignant behavior. In pancreatic ductal adenocarcinoma and endometrial carcinoma, miR-337 dysregulation is linked to altered expression of HOXB7 and PTEN, underscoring its context-dependent role in oncogenesis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "5", "end_ref": "8"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn breast cancer, the tumor-suppressive function of miR-337–3p is supported by findings that its downregulation correlates with enhanced cell viability, epithelial–mesenchymal transition, and motility—effects mediated by upregulation of targets such as ESRP1. Likewise, in cutaneous T-cell lymphoma and esophageal squamous cell carcinoma, reduced miR-337 expression is associated with increased STAT3 and JAK2 signaling, respectively. These observations emphasize how deregulation of miR-337 contributes to tumor progression across diverse malignancies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "9", "end_ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in tumor biology, miR-337 also participates in non‐oncogenic processes. In adipose tissue, its elevated expression in brown adipocytes contributes to the browning process by targeting Twist1, a negative regulator of brown fat metabolism. In another context, high-glucose conditions in bone marrow mesenchymal stem cells induce miR-337–3p expression, which in turn suppresses osteogenic differentiation via inhibition of Rap1A; such findings may have implications for diabetic osteoporosis. Moreover, in the host response to Mycobacterium tuberculosis infection, increased miR-337–3p impairs Vitamin D–dependent antimicrobial pathways by concurrently targeting the 3′UTRs of TLR4 and STAT3, thus compromising fast-acting immunity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "15"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAdditional studies have revealed that the -5p species of miR-337 can regulate NPM1 expression in acute myeloid leukemia, creating prognostic implications based on miRNA-directed suppression. In osteosarcoma, miR-337–3p is sequestered by circular RNAs such as circVRK1, which leads to de-repression of the tumor-suppressor gene ZNF652 and a consequent inhibition of cell proliferation, migration, and invasion. Similar ceRNA mechanisms involving miR-337 have been documented in other tumor types including renal cell carcinoma and non-small cell lung cancer, highlighting its diverse regulatory roles across biological systems."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "16", "end_ref": "19"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nCollectively, these studies illustrate that miR-337 operates as a multifaceted regulator. Depending on the cellular context, miR-337 (or its specific isoforms) can function as a tumor suppressor—through inhibition of oncogenic signaling (e.g., STAT3, PIK3CA/B, ESRP1) and promotion of apoptotic pathways—or, conversely, act in a pro-tumorigenic manner when its endogenous levels are altered by competing endogenous RNAs. Its roles extend beyond cancer to influence metabolic and immune responses, emphasizing the potential of miR-337 both as a biomarker and as a therapeutic target in a wide range of diseases."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "20", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Liqin Du, Maria C Subauste, Christopher DeSevo, et al. 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