{"title":"LncRNA U731166通过海绵miR-3607-3p在食管鳞癌(ESCC)中增加TGFBR1的积累,促进肿瘤转移","authors":"Mingbo Wang, Meng Wang, Chao Huang, Yonggang Zhu, Fan Zhang, Wenda Gao, Zhenhua Li, Liangbiao Peng, Ziqiang Tian, Chao Gao, Xingpeng Han","doi":"10.30498/ijb.2024.343750.3391","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Long non-coding RNA (lncRNA) U731166 and microRNA (miR)-3607-3p are two ncRNAs with critical roles in cancer biology, while their involvement in esophageal squamous-cell carcinomas (ESCC) is unclear. We predicted that U731166 and miR-3607-3p might interact with each other. This study aimed to investigate their role and interaction in ESCC.</p><p><strong>Objectives: </strong>This study was therefore conducted to explore the involvement of U731166 and miR-3607-3p in ESCC, with a focus on the interaction between them.</p><p><strong>Materials and methods: </strong>Paired ESCC and non-tumor tissue samples were recruited from 72 ESCC patients. By RT-Qpcr, level of U731166 and miR-3607-3p in paired tissues was measured. By RNA-RNA pulldown assay, the direct interaction between U731166 and miR-3607-3p was detected. U731166 overexpression or miR-3607-3p overexpression was performed to investigate their role in regulating the expression of each other. By RT-qPCR and Western blot analysis, the role of U731166 and miR-3607-3p in regulating the level of TGFBR1 was assessed. By Transwell assays, cell invasion and migration were analyzed.</p><p><strong>Results: </strong>Compared to non-tumor tissues, U731166 was highly upregulated in ESCC, while miR-3607-3p was downregulated in ESCC. U731166 and miR-3607-3p directly interacted with each other, but they are not closely correlated and did not regulate the level of each other. Moreover, U731166 reversed the role of miR-3607-3p in downregulating TGFBR1 and inhibiting cancer cell invasion and migration. U731166 and miR-3607-3p were closely associated with patients' tumor metastasis but not tumor size.</p><p><strong>Conclusion: </strong>U731166 may upregulate TGFBR1 by sponging miR-3607-3p in ESCC cells to promote tumor metastasis.</p>","PeriodicalId":14492,"journal":{"name":"Iranian Journal of Biotechnology","volume":"22 3","pages":"e3391"},"PeriodicalIF":1.6000,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11682522/pdf/","citationCount":"0","resultStr":"{\"title\":\"LncRNA U731166 Increases the Accumulation of TGFBR1 by Sponging miR-3607-3p in Esophageal Squamous-Cell Carcinomas (ESCC) to Promote Tumor Metastasis.\",\"authors\":\"Mingbo Wang, Meng Wang, Chao Huang, Yonggang Zhu, Fan Zhang, Wenda Gao, Zhenhua Li, Liangbiao Peng, Ziqiang Tian, Chao Gao, Xingpeng Han\",\"doi\":\"10.30498/ijb.2024.343750.3391\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Long non-coding RNA (lncRNA) U731166 and microRNA (miR)-3607-3p are two ncRNAs with critical roles in cancer biology, while their involvement in esophageal squamous-cell carcinomas (ESCC) is unclear. We predicted that U731166 and miR-3607-3p might interact with each other. This study aimed to investigate their role and interaction in ESCC.</p><p><strong>Objectives: </strong>This study was therefore conducted to explore the involvement of U731166 and miR-3607-3p in ESCC, with a focus on the interaction between them.</p><p><strong>Materials and methods: </strong>Paired ESCC and non-tumor tissue samples were recruited from 72 ESCC patients. By RT-Qpcr, level of U731166 and miR-3607-3p in paired tissues was measured. By RNA-RNA pulldown assay, the direct interaction between U731166 and miR-3607-3p was detected. U731166 overexpression or miR-3607-3p overexpression was performed to investigate their role in regulating the expression of each other. By RT-qPCR and Western blot analysis, the role of U731166 and miR-3607-3p in regulating the level of TGFBR1 was assessed. By Transwell assays, cell invasion and migration were analyzed.</p><p><strong>Results: </strong>Compared to non-tumor tissues, U731166 was highly upregulated in ESCC, while miR-3607-3p was downregulated in ESCC. U731166 and miR-3607-3p directly interacted with each other, but they are not closely correlated and did not regulate the level of each other. Moreover, U731166 reversed the role of miR-3607-3p in downregulating TGFBR1 and inhibiting cancer cell invasion and migration. U731166 and miR-3607-3p were closely associated with patients' tumor metastasis but not tumor size.</p><p><strong>Conclusion: </strong>U731166 may upregulate TGFBR1 by sponging miR-3607-3p in ESCC cells to promote tumor metastasis.</p>\",\"PeriodicalId\":14492,\"journal\":{\"name\":\"Iranian Journal of Biotechnology\",\"volume\":\"22 3\",\"pages\":\"e3391\"},\"PeriodicalIF\":1.6000,\"publicationDate\":\"2024-07-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11682522/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Iranian Journal of Biotechnology\",\"FirstCategoryId\":\"5\",\"ListUrlMain\":\"https://doi.org/10.30498/ijb.2024.343750.3391\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"BIOTECHNOLOGY & APPLIED MICROBIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Iranian Journal of Biotechnology","FirstCategoryId":"5","ListUrlMain":"https://doi.org/10.30498/ijb.2024.343750.3391","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOTECHNOLOGY & APPLIED MICROBIOLOGY","Score":null,"Total":0}
LncRNA U731166 Increases the Accumulation of TGFBR1 by Sponging miR-3607-3p in Esophageal Squamous-Cell Carcinomas (ESCC) to Promote Tumor Metastasis.
Background: Long non-coding RNA (lncRNA) U731166 and microRNA (miR)-3607-3p are two ncRNAs with critical roles in cancer biology, while their involvement in esophageal squamous-cell carcinomas (ESCC) is unclear. We predicted that U731166 and miR-3607-3p might interact with each other. This study aimed to investigate their role and interaction in ESCC.
Objectives: This study was therefore conducted to explore the involvement of U731166 and miR-3607-3p in ESCC, with a focus on the interaction between them.
Materials and methods: Paired ESCC and non-tumor tissue samples were recruited from 72 ESCC patients. By RT-Qpcr, level of U731166 and miR-3607-3p in paired tissues was measured. By RNA-RNA pulldown assay, the direct interaction between U731166 and miR-3607-3p was detected. U731166 overexpression or miR-3607-3p overexpression was performed to investigate their role in regulating the expression of each other. By RT-qPCR and Western blot analysis, the role of U731166 and miR-3607-3p in regulating the level of TGFBR1 was assessed. By Transwell assays, cell invasion and migration were analyzed.
Results: Compared to non-tumor tissues, U731166 was highly upregulated in ESCC, while miR-3607-3p was downregulated in ESCC. U731166 and miR-3607-3p directly interacted with each other, but they are not closely correlated and did not regulate the level of each other. Moreover, U731166 reversed the role of miR-3607-3p in downregulating TGFBR1 and inhibiting cancer cell invasion and migration. U731166 and miR-3607-3p were closely associated with patients' tumor metastasis but not tumor size.
Conclusion: U731166 may upregulate TGFBR1 by sponging miR-3607-3p in ESCC cells to promote tumor metastasis.
期刊介绍:
Iranian Journal of Biotechnology (IJB) is published quarterly by the National Institute of Genetic Engineering and Biotechnology. IJB publishes original scientific research papers in the broad area of Biotechnology such as, Agriculture, Animal and Marine Sciences, Basic Sciences, Bioinformatics, Biosafety and Bioethics, Environment, Industry and Mining and Medical Sciences.