Wei Xia, Jihe Huang, Chunhua Sun, Fei Shen, Kejia Yang
{"title":"MicroRNA-1224 通过下调脊索瘤中 CBX3 的表达抑制细胞增殖。","authors":"Wei Xia, Jihe Huang, Chunhua Sun, Fei Shen, Kejia Yang","doi":"10.3892/ol.2024.14395","DOIUrl":null,"url":null,"abstract":"MicroRNAs (miRNAs/miRs) have abnormal expression in numerous tumors and are closely related to tumor development and resistance to radiotherapy and chemotherapy. However, there are few studies assessing the role and mechanism of miRNA in chordoma. The sequencing data of three pairs of chordoma and notochord tissues from the GSE56183 dataset were analyzed in the present study. Cell proliferation was assessed <i>in vitro</i> using Cell Counting Kit-8. Bioinformatics analysis and the dual luciferase reporter assay were used to evaluate the regulatory relationship between miR-1224 and chromobox 3 (CBX3) in chordoma. The results demonstrated that miR-1224 had a significantly lower expression level in chordoma tissues and cell lines. Overexpression of miR-1224 inhibited proliferation in the chordoma cells, while the knockdown of miR-1224 promoted proliferation of the chordoma cells. Bioinformatics analysis and the dual luciferase reporter assay confirmed that CBX3 was a direct target gene of miR-1224 and that miR-1224 induced the proliferation of chordoma cells through the inhibition of CBX3. In summary, miR-1224 reduced the proliferation of chordoma cells through inhibition of CBX3, which provides a theoretical basis for selecting a novel therapeutic target for chordoma.","PeriodicalId":19503,"journal":{"name":"Oncology Letters","volume":"173 1","pages":""},"PeriodicalIF":2.5000,"publicationDate":"2024-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"MicroRNA‑1224 inhibits cell proliferation by downregulating CBX3 expression in chordoma.\",\"authors\":\"Wei Xia, Jihe Huang, Chunhua Sun, Fei Shen, Kejia Yang\",\"doi\":\"10.3892/ol.2024.14395\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"MicroRNAs (miRNAs/miRs) have abnormal expression in numerous tumors and are closely related to tumor development and resistance to radiotherapy and chemotherapy. However, there are few studies assessing the role and mechanism of miRNA in chordoma. The sequencing data of three pairs of chordoma and notochord tissues from the GSE56183 dataset were analyzed in the present study. Cell proliferation was assessed <i>in vitro</i> using Cell Counting Kit-8. Bioinformatics analysis and the dual luciferase reporter assay were used to evaluate the regulatory relationship between miR-1224 and chromobox 3 (CBX3) in chordoma. The results demonstrated that miR-1224 had a significantly lower expression level in chordoma tissues and cell lines. Overexpression of miR-1224 inhibited proliferation in the chordoma cells, while the knockdown of miR-1224 promoted proliferation of the chordoma cells. Bioinformatics analysis and the dual luciferase reporter assay confirmed that CBX3 was a direct target gene of miR-1224 and that miR-1224 induced the proliferation of chordoma cells through the inhibition of CBX3. In summary, miR-1224 reduced the proliferation of chordoma cells through inhibition of CBX3, which provides a theoretical basis for selecting a novel therapeutic target for chordoma.\",\"PeriodicalId\":19503,\"journal\":{\"name\":\"Oncology Letters\",\"volume\":\"173 1\",\"pages\":\"\"},\"PeriodicalIF\":2.5000,\"publicationDate\":\"2024-04-10\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Oncology Letters\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.3892/ol.2024.14395\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Oncology Letters","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3892/ol.2024.14395","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"ONCOLOGY","Score":null,"Total":0}
MicroRNA‑1224 inhibits cell proliferation by downregulating CBX3 expression in chordoma.
MicroRNAs (miRNAs/miRs) have abnormal expression in numerous tumors and are closely related to tumor development and resistance to radiotherapy and chemotherapy. However, there are few studies assessing the role and mechanism of miRNA in chordoma. The sequencing data of three pairs of chordoma and notochord tissues from the GSE56183 dataset were analyzed in the present study. Cell proliferation was assessed in vitro using Cell Counting Kit-8. Bioinformatics analysis and the dual luciferase reporter assay were used to evaluate the regulatory relationship between miR-1224 and chromobox 3 (CBX3) in chordoma. The results demonstrated that miR-1224 had a significantly lower expression level in chordoma tissues and cell lines. Overexpression of miR-1224 inhibited proliferation in the chordoma cells, while the knockdown of miR-1224 promoted proliferation of the chordoma cells. Bioinformatics analysis and the dual luciferase reporter assay confirmed that CBX3 was a direct target gene of miR-1224 and that miR-1224 induced the proliferation of chordoma cells through the inhibition of CBX3. In summary, miR-1224 reduced the proliferation of chordoma cells through inhibition of CBX3, which provides a theoretical basis for selecting a novel therapeutic target for chordoma.
期刊介绍:
Oncology Letters is a monthly, peer-reviewed journal, available in print and online, that focuses on all aspects of clinical oncology, as well as in vitro and in vivo experimental model systems relevant to the mechanisms of disease.
The principal aim of Oncology Letters is to provide the prompt publication of original studies of high quality that pertain to clinical oncology, chemotherapy, oncogenes, carcinogenesis, metastasis, epidemiology and viral oncology in the form of original research, reviews and case reports.