Rui-Ting Zhou, Xiao-Jie Luo, Xiao-Xin-Ran Zhang, Jiang-Feng Wu, Yi-Ran Ni
{"title":"miR-29在调节肿瘤血管生成中的潜力:一项全面的综述。","authors":"Rui-Ting Zhou, Xiao-Jie Luo, Xiao-Xin-Ran Zhang, Jiang-Feng Wu, Yi-Ran Ni","doi":"10.1007/s12672-025-02246-3","DOIUrl":null,"url":null,"abstract":"<p><p>MicroRNAs (miRNAs) are a class of short non-coding RNAs that play a crucial role in the post-transcriptional regulation of gene expression. They are associated with various biological processes related to tumors. Among the numerous miRNAs, miR-29 has garnered attention for its role in regulating tumor angiogenesis. In numerous human tumors, miR-29 has been demonstrated to negatively correlate with the capacity for angiogenesis and the degree of malignancy, as well as with the expression levels of pro-angiogenic factors such as vascular endothelial growth factor vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), and matrix metalloproteinase (MMP)-2. Multiple studies, utilizing techniques like dual-luciferase reporter assays, have confirmed that miR-29 directly targets the 3'-untranslated region (UTR) of mRNAs for VEGF, PDGF, and MMP-2. Extensive investigations involving tumor cell lines and animal models have shown that the overexpression of miR-29, achieved through miRNA transfection or the introduction of miRNA mimics, effectively inhibits angiogenesis by upregulating these pro-angiogenic factors. Conversely, downregulation of miR-29 using specific inhibitors promotes angiogenesis. While small molecule inhibitors and antibodies targeting VEGF constitute a primary strategy in anti-angiogenesis therapies, miR-29's ability to target multiple pro-angiogenic molecules positions it as a promising candidate for future therapeutic interventions, especially with ongoing advancements in nucleic acid drug design and delivery systems.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"474"},"PeriodicalIF":2.8000,"publicationDate":"2025-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11973036/pdf/","citationCount":"0","resultStr":"{\"title\":\"The potential of miR-29 in modulating tumor angiogenesis: a comprehensive review.\",\"authors\":\"Rui-Ting Zhou, Xiao-Jie Luo, Xiao-Xin-Ran Zhang, Jiang-Feng Wu, Yi-Ran Ni\",\"doi\":\"10.1007/s12672-025-02246-3\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>MicroRNAs (miRNAs) are a class of short non-coding RNAs that play a crucial role in the post-transcriptional regulation of gene expression. They are associated with various biological processes related to tumors. Among the numerous miRNAs, miR-29 has garnered attention for its role in regulating tumor angiogenesis. In numerous human tumors, miR-29 has been demonstrated to negatively correlate with the capacity for angiogenesis and the degree of malignancy, as well as with the expression levels of pro-angiogenic factors such as vascular endothelial growth factor vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), and matrix metalloproteinase (MMP)-2. Multiple studies, utilizing techniques like dual-luciferase reporter assays, have confirmed that miR-29 directly targets the 3'-untranslated region (UTR) of mRNAs for VEGF, PDGF, and MMP-2. Extensive investigations involving tumor cell lines and animal models have shown that the overexpression of miR-29, achieved through miRNA transfection or the introduction of miRNA mimics, effectively inhibits angiogenesis by upregulating these pro-angiogenic factors. Conversely, downregulation of miR-29 using specific inhibitors promotes angiogenesis. While small molecule inhibitors and antibodies targeting VEGF constitute a primary strategy in anti-angiogenesis therapies, miR-29's ability to target multiple pro-angiogenic molecules positions it as a promising candidate for future therapeutic interventions, especially with ongoing advancements in nucleic acid drug design and delivery systems.</p>\",\"PeriodicalId\":11148,\"journal\":{\"name\":\"Discover. Oncology\",\"volume\":\"16 1\",\"pages\":\"474\"},\"PeriodicalIF\":2.8000,\"publicationDate\":\"2025-04-06\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11973036/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Discover. 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The potential of miR-29 in modulating tumor angiogenesis: a comprehensive review.
MicroRNAs (miRNAs) are a class of short non-coding RNAs that play a crucial role in the post-transcriptional regulation of gene expression. They are associated with various biological processes related to tumors. Among the numerous miRNAs, miR-29 has garnered attention for its role in regulating tumor angiogenesis. In numerous human tumors, miR-29 has been demonstrated to negatively correlate with the capacity for angiogenesis and the degree of malignancy, as well as with the expression levels of pro-angiogenic factors such as vascular endothelial growth factor vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), and matrix metalloproteinase (MMP)-2. Multiple studies, utilizing techniques like dual-luciferase reporter assays, have confirmed that miR-29 directly targets the 3'-untranslated region (UTR) of mRNAs for VEGF, PDGF, and MMP-2. Extensive investigations involving tumor cell lines and animal models have shown that the overexpression of miR-29, achieved through miRNA transfection or the introduction of miRNA mimics, effectively inhibits angiogenesis by upregulating these pro-angiogenic factors. Conversely, downregulation of miR-29 using specific inhibitors promotes angiogenesis. While small molecule inhibitors and antibodies targeting VEGF constitute a primary strategy in anti-angiogenesis therapies, miR-29's ability to target multiple pro-angiogenic molecules positions it as a promising candidate for future therapeutic interventions, especially with ongoing advancements in nucleic acid drug design and delivery systems.