{"title":"通过靶向miR-601/TSPAN8信号轴研究LINC00483作为结直肠癌新致癌基因的特性","authors":"Xiao Liu, Hui Xiong, Tie Chen, Xue Qiu","doi":"10.1002/jbt.70164","DOIUrl":null,"url":null,"abstract":"<div>\n \n <p>LINC00483 is exerted a crucial function in many malignant tumors' progression, but the role of LINC00483 in colorectal cancer (CRC) carcinogenesis remains not fully understood. The aim of our study was to explore the potential role of LINC00483 in the development of CRC and its underlying molecular mechanism. In the present study, the level of mRNA and protein was assessed through using qRT-PCR and Western blot analysis assays. Cell proliferation was assessed by using Cell Counting Kit-8 (CCK-8) and colony formation assays. The cell metastasis was assessed by using transwell assays. Results revealed that LINC00483 was elevated in CRC tissue and cell lines. Upregulation of LINC00483 was negatively correlated with the overall survival. The mRNA expression of tetraspanin 8 (TSPAN8) is increased in CRC tissues, whereas the expression of miR-601 is decreased, and in CRC tissues, a correlation between the expression levels of LINC00483 and TSPAN8 was positive, but the correlation between LINC00483 and miR-601 was negative. LINC00483 deficiency could inhibit the cell proliferation, migration, and invasion in CRC cell lines. Moreover, the proliferation, migration, and invasion were inhibited in CRC cell lines after transfected with miR-601 mimics; but this effect could be eliminated by LINC00483 overexpressed. Results also suggested that the protein expression of TSPAN8 and N-cadherin is decreased in CRC cell lines after transfected with miR-601 mimics, whereas the protein expression of E-cadherin is increased; but this effect could be abrogated by LINC00483 overexpressed, which means that miR-601 mimics can inhibit the metastasis of CRC, but after cotransfection with LINC00483, the metastasis ability of CRC is restored. In conclusion, our study elucidated that LINC00483 promote the CRC progression by upregulating TSPAN8 via sponging miR-601. This finding provided a new potential drug target for the treatment of CRC in clinic.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 3","pages":""},"PeriodicalIF":3.2000,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Characterization of LINC00483 as a Novel Oncogene in Colorectal Cancer via Targeting miR-601/TSPAN8 Signaling Axis\",\"authors\":\"Xiao Liu, Hui Xiong, Tie Chen, Xue Qiu\",\"doi\":\"10.1002/jbt.70164\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n <p>LINC00483 is exerted a crucial function in many malignant tumors' progression, but the role of LINC00483 in colorectal cancer (CRC) carcinogenesis remains not fully understood. The aim of our study was to explore the potential role of LINC00483 in the development of CRC and its underlying molecular mechanism. In the present study, the level of mRNA and protein was assessed through using qRT-PCR and Western blot analysis assays. Cell proliferation was assessed by using Cell Counting Kit-8 (CCK-8) and colony formation assays. The cell metastasis was assessed by using transwell assays. Results revealed that LINC00483 was elevated in CRC tissue and cell lines. Upregulation of LINC00483 was negatively correlated with the overall survival. The mRNA expression of tetraspanin 8 (TSPAN8) is increased in CRC tissues, whereas the expression of miR-601 is decreased, and in CRC tissues, a correlation between the expression levels of LINC00483 and TSPAN8 was positive, but the correlation between LINC00483 and miR-601 was negative. LINC00483 deficiency could inhibit the cell proliferation, migration, and invasion in CRC cell lines. Moreover, the proliferation, migration, and invasion were inhibited in CRC cell lines after transfected with miR-601 mimics; but this effect could be eliminated by LINC00483 overexpressed. Results also suggested that the protein expression of TSPAN8 and N-cadherin is decreased in CRC cell lines after transfected with miR-601 mimics, whereas the protein expression of E-cadherin is increased; but this effect could be abrogated by LINC00483 overexpressed, which means that miR-601 mimics can inhibit the metastasis of CRC, but after cotransfection with LINC00483, the metastasis ability of CRC is restored. In conclusion, our study elucidated that LINC00483 promote the CRC progression by upregulating TSPAN8 via sponging miR-601. This finding provided a new potential drug target for the treatment of CRC in clinic.</p></div>\",\"PeriodicalId\":15151,\"journal\":{\"name\":\"Journal of Biochemical and Molecular Toxicology\",\"volume\":\"39 3\",\"pages\":\"\"},\"PeriodicalIF\":3.2000,\"publicationDate\":\"2025-03-10\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Biochemical and Molecular Toxicology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1002/jbt.70164\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Biochemical and Molecular Toxicology","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/jbt.70164","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
Characterization of LINC00483 as a Novel Oncogene in Colorectal Cancer via Targeting miR-601/TSPAN8 Signaling Axis
LINC00483 is exerted a crucial function in many malignant tumors' progression, but the role of LINC00483 in colorectal cancer (CRC) carcinogenesis remains not fully understood. The aim of our study was to explore the potential role of LINC00483 in the development of CRC and its underlying molecular mechanism. In the present study, the level of mRNA and protein was assessed through using qRT-PCR and Western blot analysis assays. Cell proliferation was assessed by using Cell Counting Kit-8 (CCK-8) and colony formation assays. The cell metastasis was assessed by using transwell assays. Results revealed that LINC00483 was elevated in CRC tissue and cell lines. Upregulation of LINC00483 was negatively correlated with the overall survival. The mRNA expression of tetraspanin 8 (TSPAN8) is increased in CRC tissues, whereas the expression of miR-601 is decreased, and in CRC tissues, a correlation between the expression levels of LINC00483 and TSPAN8 was positive, but the correlation between LINC00483 and miR-601 was negative. LINC00483 deficiency could inhibit the cell proliferation, migration, and invasion in CRC cell lines. Moreover, the proliferation, migration, and invasion were inhibited in CRC cell lines after transfected with miR-601 mimics; but this effect could be eliminated by LINC00483 overexpressed. Results also suggested that the protein expression of TSPAN8 and N-cadherin is decreased in CRC cell lines after transfected with miR-601 mimics, whereas the protein expression of E-cadherin is increased; but this effect could be abrogated by LINC00483 overexpressed, which means that miR-601 mimics can inhibit the metastasis of CRC, but after cotransfection with LINC00483, the metastasis ability of CRC is restored. In conclusion, our study elucidated that LINC00483 promote the CRC progression by upregulating TSPAN8 via sponging miR-601. This finding provided a new potential drug target for the treatment of CRC in clinic.
期刊介绍：
The Journal of Biochemical and Molecular Toxicology is an international journal that contains original research papers, rapid communications, mini-reviews, and book reviews, all focusing on the molecular mechanisms of action and detoxication of exogenous and endogenous chemicals and toxic agents. The scope includes effects on the organism at all stages of development, on organ systems, tissues, and cells as well as on enzymes, receptors, hormones, and genes. The biochemical and molecular aspects of uptake, transport, storage, excretion, lactivation and detoxication of drugs, agricultural, industrial and environmental chemicals, natural products and food additives are all subjects suitable for publication. Of particular interest are aspects of molecular biology related to biochemical toxicology. These include studies of the expression of genes related to detoxication and activation enzymes, toxicants with modes of action involving effects on nucleic acids, gene expression and protein synthesis, and the toxicity of products derived from biotechnology.
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