Yuanyuan Zhang, Anni Xu, Huiling Qin, Dongcai Feng, Changyu Tian, Caiqin Lin
{"title":"miR-330-3p Inhibits the Development of Acute Myeloid Leukemia by Targeting SYTL4","authors":"Yuanyuan Zhang, Anni Xu, Huiling Qin, Dongcai Feng, Changyu Tian, Caiqin Lin","doi":"10.1111/apm.70237","DOIUrl":null,"url":null,"abstract":"<div>\n \n <p>MicroRNAs (miRNAs) serve as crucial regulators in the development of various cancers. Studies have mentioned that miR-330-3p is reduced in Acute myeloid leukemia (AML). Our research objectives included determining the regulatory roles and underlying mechanisms of miR-330-3p in AML progression. miR-330-3p expression in AML was quantified through qRT-PCR. The clinical relevance of miR-330-3p in AML progression, diagnosis, and prognosis was assessed by chi-square, ROC, Cox, and Kaplan–Meier survival analysis. The impacts of miR-330-3p on AML cell function were examined by CCK8 and Transwell assay. The targeting relationship between miR-330-3p and SYTL4 was analyzed via database and luciferase assay. miR-330-3p was obviously reduced in AML. Low miR-330-3p expression was related to adverse clinical features of AML, suggesting AML progression. miR-330-3p performed well in differentiating AML patients from healthy individuals, and reduced miR-330-3p expression was significantly related to poorer survival outcomes in patients with AML. miR-330-3p upregulation potently inhibited AML cell proliferation, migration, and invasion. Furthermore, SYTL4 was a target gene of miR-330-3p. And rescue tests demonstrated that miR-330-3p and SYTL4 jointly participate in the development of AML. In conclusion, miR-330-3p inhibited the development of AML by targeting SYTL4; miR-330-3p may serve as a valuable prognosis and diagnostic biomarker for AML patients.</p>\n </div>","PeriodicalId":8167,"journal":{"name":"Apmis","volume":"134 7","pages":""},"PeriodicalIF":2.2000,"publicationDate":"2026-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Apmis","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/apm.70237","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
MicroRNAs (miRNAs) serve as crucial regulators in the development of various cancers. Studies have mentioned that miR-330-3p is reduced in Acute myeloid leukemia (AML). Our research objectives included determining the regulatory roles and underlying mechanisms of miR-330-3p in AML progression. miR-330-3p expression in AML was quantified through qRT-PCR. The clinical relevance of miR-330-3p in AML progression, diagnosis, and prognosis was assessed by chi-square, ROC, Cox, and Kaplan–Meier survival analysis. The impacts of miR-330-3p on AML cell function were examined by CCK8 and Transwell assay. The targeting relationship between miR-330-3p and SYTL4 was analyzed via database and luciferase assay. miR-330-3p was obviously reduced in AML. Low miR-330-3p expression was related to adverse clinical features of AML, suggesting AML progression. miR-330-3p performed well in differentiating AML patients from healthy individuals, and reduced miR-330-3p expression was significantly related to poorer survival outcomes in patients with AML. miR-330-3p upregulation potently inhibited AML cell proliferation, migration, and invasion. Furthermore, SYTL4 was a target gene of miR-330-3p. And rescue tests demonstrated that miR-330-3p and SYTL4 jointly participate in the development of AML. In conclusion, miR-330-3p inhibited the development of AML by targeting SYTL4; miR-330-3p may serve as a valuable prognosis and diagnostic biomarker for AML patients.
期刊介绍:
APMIS, formerly Acta Pathologica, Microbiologica et Immunologica Scandinavica, has been published since 1924 by the Scandinavian Societies for Medical Microbiology and Pathology as a non-profit-making scientific journal.