{"title":"长非编码 RNA MAFG-AS1 通过与 miR-331-3p 竞争性结合，促进 KIT 的表达，从而增强黑色素瘤细胞的增殖、侵袭和上皮-间质转化能力","authors":"Zongjiang Yao, Peiwu Li, Hong Liu","doi":"10.1007/s13273-023-00409-3","DOIUrl":null,"url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Objective</h3><p>Melanoma is a malignant skin cancer. This paper is dedicated to investigate the disease mechanism in regard to the axis of long noncoding RNA MAFG antisense 1 (MAFG-AS1)/microRNA (miR)-331-3p/KIT.</p><h3 data-test=\"abstract-sub-heading\">Methods</h3><p>Levels of MAFG-AS1, miR-331-3p and KIT were analyzed in melanoma patients' cancer tissues and melanocytic nevi patients’ skin tissues. The correlation between prognosis of melanoma patients with MAFG-AS1 expression was observed. Loss- and gain-function tests were implemented to observe alternatives of cell biological activities.</p><h3 data-test=\"abstract-sub-heading\">Results</h3><p>Melanoma patients’ cancer tissues expressed higher MAFG-AS1 and KIT and lower miR-331-3p. Patients with high MAFG-AS1 expression exhibited a poorer prognosis. After down-regulating MAFG-AS1 in A375 cells, cell proliferation, invasiveness, epithelial–mesenchymal transition (EMT) decreased, and apoptosis increased. Up-regulating MAFG-AS1 caused the opposite consequences. miR-331-3p inhibition or KIT overexpression eliminated the blockade of proliferation, invasion, and EMT caused by MAFG-AS1 silencing.</p><h3 data-test=\"abstract-sub-heading\">Conclusion</h3><p>MAFG-AS1 competitively binds to miR-331-3p to elevate KIT expression, thereby enhancing the aggressiveness of melanoma cells.</p>","PeriodicalId":18683,"journal":{"name":"Molecular & Cellular Toxicology","volume":"138 1","pages":""},"PeriodicalIF":1.1000,"publicationDate":"2023-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Long noncoding RNA MAFG-AS1 enhances proliferation, invasion, and epithelial–mesenchymal transition of melanoma cells through promoting KIT expression by competitively binding to miR-331-3p\",\"authors\":\"Zongjiang Yao, Peiwu Li, Hong Liu\",\"doi\":\"10.1007/s13273-023-00409-3\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<h3 data-test=\\\"abstract-sub-heading\\\">Objective</h3><p>Melanoma is a malignant skin cancer. This paper is dedicated to investigate the disease mechanism in regard to the axis of long noncoding RNA MAFG antisense 1 (MAFG-AS1)/microRNA (miR)-331-3p/KIT.</p><h3 data-test=\\\"abstract-sub-heading\\\">Methods</h3><p>Levels of MAFG-AS1, miR-331-3p and KIT were analyzed in melanoma patients' cancer tissues and melanocytic nevi patients’ skin tissues. The correlation between prognosis of melanoma patients with MAFG-AS1 expression was observed. Loss- and gain-function tests were implemented to observe alternatives of cell biological activities.</p><h3 data-test=\\\"abstract-sub-heading\\\">Results</h3><p>Melanoma patients’ cancer tissues expressed higher MAFG-AS1 and KIT and lower miR-331-3p. Patients with high MAFG-AS1 expression exhibited a poorer prognosis. After down-regulating MAFG-AS1 in A375 cells, cell proliferation, invasiveness, epithelial–mesenchymal transition (EMT) decreased, and apoptosis increased. Up-regulating MAFG-AS1 caused the opposite consequences. miR-331-3p inhibition or KIT overexpression eliminated the blockade of proliferation, invasion, and EMT caused by MAFG-AS1 silencing.</p><h3 data-test=\\\"abstract-sub-heading\\\">Conclusion</h3><p>MAFG-AS1 competitively binds to miR-331-3p to elevate KIT expression, thereby enhancing the aggressiveness of melanoma cells.</p>\",\"PeriodicalId\":18683,\"journal\":{\"name\":\"Molecular & Cellular Toxicology\",\"volume\":\"138 1\",\"pages\":\"\"},\"PeriodicalIF\":1.1000,\"publicationDate\":\"2023-12-07\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Molecular & Cellular Toxicology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1007/s13273-023-00409-3\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"TOXICOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular & Cellular Toxicology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s13273-023-00409-3","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"TOXICOLOGY","Score":null,"Total":0}
Long noncoding RNA MAFG-AS1 enhances proliferation, invasion, and epithelial–mesenchymal transition of melanoma cells through promoting KIT expression by competitively binding to miR-331-3p
Objective
Melanoma is a malignant skin cancer. This paper is dedicated to investigate the disease mechanism in regard to the axis of long noncoding RNA MAFG antisense 1 (MAFG-AS1)/microRNA (miR)-331-3p/KIT.
Methods
Levels of MAFG-AS1, miR-331-3p and KIT were analyzed in melanoma patients' cancer tissues and melanocytic nevi patients’ skin tissues. The correlation between prognosis of melanoma patients with MAFG-AS1 expression was observed. Loss- and gain-function tests were implemented to observe alternatives of cell biological activities.
Results
Melanoma patients’ cancer tissues expressed higher MAFG-AS1 and KIT and lower miR-331-3p. Patients with high MAFG-AS1 expression exhibited a poorer prognosis. After down-regulating MAFG-AS1 in A375 cells, cell proliferation, invasiveness, epithelial–mesenchymal transition (EMT) decreased, and apoptosis increased. Up-regulating MAFG-AS1 caused the opposite consequences. miR-331-3p inhibition or KIT overexpression eliminated the blockade of proliferation, invasion, and EMT caused by MAFG-AS1 silencing.
Conclusion
MAFG-AS1 competitively binds to miR-331-3p to elevate KIT expression, thereby enhancing the aggressiveness of melanoma cells.
期刊介绍：
Molecular & Cellular Toxicology publishes original research and reviews in all areas of the complex interaction between the cell´s genome (the sum of all genes within the chromosome), chemicals in the environment, and disease. Acceptable manuscripts are the ones that deal with some topics of environmental contaminants, including those that lie in the domains of analytical chemistry, biochemistry, pharmacology and toxicology with the aspects of molecular and cellular levels. Emphasis will be placed on toxic effects observed at relevant genomics and proteomics, which have direct impact on drug development, environment health, food safety, preventive medicine, and forensic medicine. The journal is committed to rapid peer review to ensure the publication of highest quality original research and timely news and review articles.
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