Yu Zi Ji, Yu Jie Wang, Ji Qing Ma, Zhi Hua Yin, Fei Liu, Yan Zi Zang, Guang Ke Wang, Yong Tai
{"title":"miR-34c-3p通过抑制巨噬细胞M2极化抑制鼻咽癌的发展。","authors":"Yu Zi Ji, Yu Jie Wang, Ji Qing Ma, Zhi Hua Yin, Fei Liu, Yan Zi Zang, Guang Ke Wang, Yong Tai","doi":"10.3967/bes2024.136","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>miR-34c-3p is down-regulated in nasopharyngeal carcinoma (NPC). The biological role of miR-34c-3p in NPC and its underlying mechanisms are unknown and were explored in this study.</p><p><strong>Methods: </strong>Flow cytometry and immunohistochemical staining were employed to detect cluster of differentiation 86 (CD86) and cluster of differentiation 206 (CD206) expression; quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting were employed to examine mRNA expression and protein levels; cell counting kit-8 (CCK8) and transwell assays were employed to assess cell proliferation, migration, and invasion; and hematoxylin-eosin (HE) staining was employed to assess pathological changes in tumor tissues.</p><p><strong>Results: </strong>Our results revealed that the miR-34c-3p mimic markedly inhibited M2 polarization of macrophages by targeting SLC7A11, and M2 macrophages transfected with the miR-34c-3p mimic inhibited the proliferation, migration, and invasion of NPC cells. The <i>in vivo</i> experiments further confirmed that miR-34c-3p mimics blocked tumor growth and reduced inflammatory infiltration in tumor tissues.</p><p><strong>Conclusion: </strong>This study provides novel insights into the pathogenesis of NPC and a new treatment strategy.</p>","PeriodicalId":93903,"journal":{"name":"Biomedical and environmental sciences : BES","volume":"38 2","pages":"219-229"},"PeriodicalIF":0.0000,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"miR-34c-3p Inhibits Nasopharyngeal Carcinoma Development <i>via</i> Inhibiting M2 Polarization of Macrophages.\",\"authors\":\"Yu Zi Ji, Yu Jie Wang, Ji Qing Ma, Zhi Hua Yin, Fei Liu, Yan Zi Zang, Guang Ke Wang, Yong Tai\",\"doi\":\"10.3967/bes2024.136\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>miR-34c-3p is down-regulated in nasopharyngeal carcinoma (NPC). The biological role of miR-34c-3p in NPC and its underlying mechanisms are unknown and were explored in this study.</p><p><strong>Methods: </strong>Flow cytometry and immunohistochemical staining were employed to detect cluster of differentiation 86 (CD86) and cluster of differentiation 206 (CD206) expression; quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting were employed to examine mRNA expression and protein levels; cell counting kit-8 (CCK8) and transwell assays were employed to assess cell proliferation, migration, and invasion; and hematoxylin-eosin (HE) staining was employed to assess pathological changes in tumor tissues.</p><p><strong>Results: </strong>Our results revealed that the miR-34c-3p mimic markedly inhibited M2 polarization of macrophages by targeting SLC7A11, and M2 macrophages transfected with the miR-34c-3p mimic inhibited the proliferation, migration, and invasion of NPC cells. The <i>in vivo</i> experiments further confirmed that miR-34c-3p mimics blocked tumor growth and reduced inflammatory infiltration in tumor tissues.</p><p><strong>Conclusion: </strong>This study provides novel insights into the pathogenesis of NPC and a new treatment strategy.</p>\",\"PeriodicalId\":93903,\"journal\":{\"name\":\"Biomedical and environmental sciences : BES\",\"volume\":\"38 2\",\"pages\":\"219-229\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2025-02-20\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Biomedical and environmental sciences : BES\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.3967/bes2024.136\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biomedical and environmental sciences : BES","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3967/bes2024.136","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
miR-34c-3p Inhibits Nasopharyngeal Carcinoma Development via Inhibiting M2 Polarization of Macrophages.
Objective: miR-34c-3p is down-regulated in nasopharyngeal carcinoma (NPC). The biological role of miR-34c-3p in NPC and its underlying mechanisms are unknown and were explored in this study.
Methods: Flow cytometry and immunohistochemical staining were employed to detect cluster of differentiation 86 (CD86) and cluster of differentiation 206 (CD206) expression; quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting were employed to examine mRNA expression and protein levels; cell counting kit-8 (CCK8) and transwell assays were employed to assess cell proliferation, migration, and invasion; and hematoxylin-eosin (HE) staining was employed to assess pathological changes in tumor tissues.
Results: Our results revealed that the miR-34c-3p mimic markedly inhibited M2 polarization of macrophages by targeting SLC7A11, and M2 macrophages transfected with the miR-34c-3p mimic inhibited the proliferation, migration, and invasion of NPC cells. The in vivo experiments further confirmed that miR-34c-3p mimics blocked tumor growth and reduced inflammatory infiltration in tumor tissues.
Conclusion: This study provides novel insights into the pathogenesis of NPC and a new treatment strategy.