{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‐638 has been reported to act as a potent tumor‐suppressive microRNA in several solid tumors and hematologic malignancies. In hepatocellular carcinoma, colorectal carcinoma, and oral squamous cell carcinoma, reduced miR‐638 expression correlates with enhanced proliferation, invasion, migration, angiogenesis, and poor patient prognosis; mechanistic studies revealed that miR‐638 suppresses tumorigenesis by targeting oncogenic factors such as TSPAN1, VEGF, SOX2, and MACC1. Moreover, in acute myeloid leukemia models, miR‐638 overexpression promoted myeloid differentiation and induced G1 cell cycle arrest by targeting cyclin‐dependent kinases. These findings collectively suggest an important tumor‐suppressive role for miR‐638 in controlling cell cycle progression, metastasis, and angiogenesis across diverse cancer types."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nConversely, evidence from other studies indicates that miR‐638 can also display oncogenic properties depending on the tumor context. In metastatic melanoma, miR‐638 is overexpressed and contributes to tumor progression by repressing p53‐mediated apoptosis, while in some non–small cell lung cancer and breast cancer models, decreased levels of miR‐638 are linked with chemoresistance and enhanced aggressive behavior. Further investigations in breast cancer stem cells, acute lymphoblastic leukemia, and cervical or ovarian malignancies also implicate dysregulation of miR‐638—whether by direct targeting of tumor suppressors such as BRCA1 or via interactions with oncogenic signaling cascades—as a factor that modulates proliferation, invasion, and drug response."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "21"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its direct roles in tumor cells, miR‐638 is increasingly recognized as a key regulator in non‐malignant contexts and in intercellular communication. Studies in vascular and airway smooth muscle cells have demonstrated that miR‐638 can impede aberrant cell proliferation and migration by targeting cell cycle regulators. In addition, miR‐638 is modulated during embryonic development, contributes to the regulation of osteogenic differentiation in aortic valve interstitial cells through targeting transcription factors such as Sp7, and influences DNA damage repair processes and chemosensitivity—potentially by interfering with the recruitment of repair proteins. Furthermore, miR‐638 can be actively secreted in exosomes or sequestered by circular RNAs, thereby affecting its bioavailability and downstream regulation in recipient cells. These multifaceted roles highlight miR‐638 as both a promising biomarker and a potential therapeutic target across a spectrum of physiologic and pathologic conditions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "22", "end_ref": "32"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jiwei Zhang, Bojian Fei, Qifeng Wang, et al. 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