{"title":"miR-203通过调控DUSP5的表达抑制胰腺癌细胞的增殖和迁移","authors":"Zekiye Altan, Yunus Sahin","doi":"10.1016/j.mcp.2022.101866","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><p>Pancreatic cancer<span> (PC) is an insidious cancer that is commonly diagnosed in advanced stages. Therefore, it is necessary to understand PC-related mechanisms in order to discover new and reliable diagnostic biomarkers. It is known that miRNAs<span> play a crucial role in carcinogenesis by targeting mRNAs. In this study we aimed to explore interaction between downregulated miR-203 and its upregulated target DUSP5 in PC.</span></span></p></div><div><h3>Methods</h3><p>Using bioinformatics approaches we identified the DUSP5 as a direct target gene of miR-203 and detected potential binding sites between miR-203 and DUSP5. Additionally, we evaluated subcellular location, expression level and prognostic value of DUSP5 in PC through using various bioinformatics tools. To investigate the relationship between miR-203 and DUSP5, we increased the expression levels of miR-203 by transfecting miR-203 mimics into the pancreatic cancer cell line, PANC-1. Finally, MTT, wound healing, and colony formation assays were performed to determine effect of overexpressed miR-203 on proliferation and migration of PANC-1 cells.</p></div><div><h3>Results</h3><p>We found that expression level of DUSP5 in pancreas tissue<span> was one of the lowest tissue expression among all normal human tissue types. In addition, DUSP5 expression was upregulated both PC tissues and cell line and associated with poor overall survival in PC. Overexpression of miR-203 significantly downregulated expression level of DUSP5 and remarkably suppressed proliferation, migration and colony formation ability of PANC-1 cells.</span></p></div><div><h3>Conclusions</h3><p>These findings suggest that miR-203 restrains proliferation and migration of PC cells by regulating oncogenic activity of DUSP5 in PC, thereby could be novel candidate biomarkers for PC diagnosis and treatment.</p></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"66 ","pages":"Article 101866"},"PeriodicalIF":2.3000,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"10","resultStr":"{\"title\":\"miR-203 suppresses pancreatic cancer cell proliferation and migration by modulating DUSP5 expression\",\"authors\":\"Zekiye Altan, Yunus Sahin\",\"doi\":\"10.1016/j.mcp.2022.101866\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Background</h3><p>Pancreatic cancer<span> (PC) is an insidious cancer that is commonly diagnosed in advanced stages. Therefore, it is necessary to understand PC-related mechanisms in order to discover new and reliable diagnostic biomarkers. It is known that miRNAs<span> play a crucial role in carcinogenesis by targeting mRNAs. In this study we aimed to explore interaction between downregulated miR-203 and its upregulated target DUSP5 in PC.</span></span></p></div><div><h3>Methods</h3><p>Using bioinformatics approaches we identified the DUSP5 as a direct target gene of miR-203 and detected potential binding sites between miR-203 and DUSP5. Additionally, we evaluated subcellular location, expression level and prognostic value of DUSP5 in PC through using various bioinformatics tools. To investigate the relationship between miR-203 and DUSP5, we increased the expression levels of miR-203 by transfecting miR-203 mimics into the pancreatic cancer cell line, PANC-1. Finally, MTT, wound healing, and colony formation assays were performed to determine effect of overexpressed miR-203 on proliferation and migration of PANC-1 cells.</p></div><div><h3>Results</h3><p>We found that expression level of DUSP5 in pancreas tissue<span> was one of the lowest tissue expression among all normal human tissue types. In addition, DUSP5 expression was upregulated both PC tissues and cell line and associated with poor overall survival in PC. Overexpression of miR-203 significantly downregulated expression level of DUSP5 and remarkably suppressed proliferation, migration and colony formation ability of PANC-1 cells.</span></p></div><div><h3>Conclusions</h3><p>These findings suggest that miR-203 restrains proliferation and migration of PC cells by regulating oncogenic activity of DUSP5 in PC, thereby could be novel candidate biomarkers for PC diagnosis and treatment.</p></div>\",\"PeriodicalId\":49799,\"journal\":{\"name\":\"Molecular and Cellular Probes\",\"volume\":\"66 \",\"pages\":\"Article 101866\"},\"PeriodicalIF\":2.3000,\"publicationDate\":\"2022-12-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"10\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Molecular and Cellular Probes\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0890850822000779\",\"RegionNum\":3,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"BIOCHEMICAL RESEARCH METHODS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular and Cellular Probes","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0890850822000779","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOCHEMICAL RESEARCH METHODS","Score":null,"Total":0}
miR-203 suppresses pancreatic cancer cell proliferation and migration by modulating DUSP5 expression
Background
Pancreatic cancer (PC) is an insidious cancer that is commonly diagnosed in advanced stages. Therefore, it is necessary to understand PC-related mechanisms in order to discover new and reliable diagnostic biomarkers. It is known that miRNAs play a crucial role in carcinogenesis by targeting mRNAs. In this study we aimed to explore interaction between downregulated miR-203 and its upregulated target DUSP5 in PC.
Methods
Using bioinformatics approaches we identified the DUSP5 as a direct target gene of miR-203 and detected potential binding sites between miR-203 and DUSP5. Additionally, we evaluated subcellular location, expression level and prognostic value of DUSP5 in PC through using various bioinformatics tools. To investigate the relationship between miR-203 and DUSP5, we increased the expression levels of miR-203 by transfecting miR-203 mimics into the pancreatic cancer cell line, PANC-1. Finally, MTT, wound healing, and colony formation assays were performed to determine effect of overexpressed miR-203 on proliferation and migration of PANC-1 cells.
Results
We found that expression level of DUSP5 in pancreas tissue was one of the lowest tissue expression among all normal human tissue types. In addition, DUSP5 expression was upregulated both PC tissues and cell line and associated with poor overall survival in PC. Overexpression of miR-203 significantly downregulated expression level of DUSP5 and remarkably suppressed proliferation, migration and colony formation ability of PANC-1 cells.
Conclusions
These findings suggest that miR-203 restrains proliferation and migration of PC cells by regulating oncogenic activity of DUSP5 in PC, thereby could be novel candidate biomarkers for PC diagnosis and treatment.
期刊介绍：
MCP - Advancing biology through–omics and bioinformatic technologies wants to capture outcomes from the current revolution in molecular technologies and sciences. The journal has broadened its scope and embraces any high quality research papers, reviews and opinions in areas including, but not limited to, molecular biology, cell biology, biochemistry, immunology, physiology, epidemiology, ecology, virology, microbiology, parasitology, genetics, evolutionary biology, genomics (including metagenomics), bioinformatics, proteomics, metabolomics, glycomics, and lipidomics. Submissions with a technology-driven focus on understanding normal biological or disease processes as well as conceptual advances and paradigm shifts are particularly encouraged. The Editors welcome fundamental or applied research areas; pre-submission enquiries about advanced draft manuscripts are welcomed. Top quality research and manuscripts will be fast-tracked.
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