{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nRecent studies have uncovered that miR-3194 plays a multifaceted role in modulating cancer stem cell phenotypes, notably in the context of human papillomavirus (HPV)‐associated oropharyngeal squamous cell carcinoma (OPSCC). In HPV16-positive cells, miR-3194-5p is upregulated in the migratory (CD44high/EpCAMlow) cancer stem cell population, and its aberrant expression correlates with increased metastatic potential. These findings suggest that miR-3194-5p may serve as a promising biomarker and therapeutic target to block metastasis in HPV-driven malignancies."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": ""}, {"type": "p", "children": [{"type": "t", "text": "\nIn esophageal cancer, miR-3194-3p has been identified as an integral component of a competing endogenous RNA network involving the long noncoding RNA KCNMB2-AS1. Here, KCNMB2-AS1 sequesters miR-3194-3p, thereby relieving miR-3194-3p-mediated repression of its target gene PYGL. The upregulation of PYGL in this axis contributes to enhanced cell proliferation, invasion, migration, and maintenance of stemness features, implicating miR-3194-3p as a key regulator in esophageal tumorigenesis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": ""}, {"type": "p", "children": [{"type": "t", "text": "\nAdditionally, miR-3194-5p has been implicated in the modulation of vascular endothelial cell function under hypoxic conditions, a critical component of coronary heart disease pathology. In hypoxia-exposed human umbilical vein endothelial cells (HUVECs), LINC00926 is highly expressed and acts by binding miR-3194-5p. This interaction disrupts the suppression of JAK1, leading to enhanced JAK1/STAT3 signaling, which in turn impairs cell proliferation, migration, tube formation, and promotes apoptosis. Such findings not only underscore the role of miR-3194-5p in endothelial dysfunction but also provide insights into its potential as a therapeutic target in vascular disease"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}]}]}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Martin Hufbauer, Margaret Maltseva, Jeannine Meinrath, et al. "}, {"type": "b", "children": [{"type": "t", "text": "HPV16 increases the number of migratory cancer stem cells and modulates their miRNA expression profile in oropharyngeal cancer."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Int J Cancer (2018)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1002/ijc.31538"}], "href": "https://doi.org/10.1002/ijc.31538"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "29663357"}], "href": "https://pubmed.ncbi.nlm.nih.gov/29663357"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Jiwen Xu, Xiaoyan Liu, Xueting Liu, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Long noncoding RNA KCNMB2-AS1 promotes the development of esophageal cancer by modulating the miR-3194-3p/PYGL axis."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Bioengineered (2021)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1080/21655979.2021.1973775"}], "href": "https://doi.org/10.1080/21655979.2021.1973775"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "34516362"}], "href": "https://pubmed.ncbi.nlm.nih.gov/34516362"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Yong Jiang, Chun-Hui Xu, Ying Zhao, et al. "}, {"type": "b", "children": [{"type": "t", "text": "LINC00926 is involved in hypoxia-induced vascular endothelial cell dysfunction "}, {"type": "a", "children": [{"type": "t", "text": "i"}], "href": "i"}, {"type": "t", "text": "via"}, {"type": "a", "children": [{"type": "t", "text": "/i"}], "href": "/i"}, {"type": "t", "text": " miR-3194-5p regulating JAK1/STAT3 signaling pathway."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Eur J Histochem (2023)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.4081/ejh.2023.3526"}], "href": "https://doi.org/10.4081/ejh.2023.3526"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "36647631"}], "href": "https://pubmed.ncbi.nlm.nih.gov/36647631"}]}]}]}