{"title":"Hsa_circ_0000105 promotes nasopharyngeal carcinoma malignancy by miR-541-3p/S100A11 axis","authors":"LuXing Peng , Jian Qin , DeFeng Qing , XinJun Huang , XiuRong Huang","doi":"10.1016/j.clinsp.2025.100577","DOIUrl":null,"url":null,"abstract":"<div><h3>Objective</h3><div>This study was to investigate whether hsa_circ_0000105 is involved in the process of regulating Nasopharyngeal Carcinoma (NPC) biological behaviors and to reveal the molecular mechanism.</div></div><div><h3>Methods</h3><div>NPC tissues and normal tissues were collected, and NPC cell lines and normal control cell lines were obtained. hsa_circ_0000105/miR-541-3p/S100A11 was evaluated by RT-qPCR or Western blot. CCK-8 assay, EdU assay, Transwell assay, wound healing assay, flow cytometry, and Western blot were employed to evaluate the biological behaviors of NPC cells. Dual luciferase reporter assay and RIP assay were applied to evaluate the direct targeting relationship of hsa_circ_0000105/miR-541-3p/S100A11. A tumor xenotransplantation assay was implemented to evaluate the effect of hsa_circ_0000105 on NPC tumors.</div></div><div><h3>Results</h3><div>hsa_circ_0000105 and S100A11 were highly expressed in NPC, while miR-541-3p was lowly expressed. hsa_circ_0000105 competitively adsorbed miR-541-3p and mediated S100A11 expression. Silencing or upregulation of hsa_circ_0000105 restricts and induces malignant behavior in HNE2 cells, respectively. The impact of hsa_circ_0000105 silencing on malignant behaviors of HNE2 cells was blocked by miR-541-3p downregulation, while that of hsa_circ_0000105 upregulation was attenuated by S100A11 inhibition.</div></div><div><h3>Conclusion</h3><div>hsa_circ_0000105 acts as a carcinogenic factor in NPC and promotes NPC malignancy by miR-541-3p/S100A11 axis.</div></div>","PeriodicalId":10472,"journal":{"name":"Clinics","volume":"80 ","pages":"Article 100577"},"PeriodicalIF":2.2000,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinics","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1807593225000031","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
引用次数: 0
Abstract
Objective
This study was to investigate whether hsa_circ_0000105 is involved in the process of regulating Nasopharyngeal Carcinoma (NPC) biological behaviors and to reveal the molecular mechanism.
Methods
NPC tissues and normal tissues were collected, and NPC cell lines and normal control cell lines were obtained. hsa_circ_0000105/miR-541-3p/S100A11 was evaluated by RT-qPCR or Western blot. CCK-8 assay, EdU assay, Transwell assay, wound healing assay, flow cytometry, and Western blot were employed to evaluate the biological behaviors of NPC cells. Dual luciferase reporter assay and RIP assay were applied to evaluate the direct targeting relationship of hsa_circ_0000105/miR-541-3p/S100A11. A tumor xenotransplantation assay was implemented to evaluate the effect of hsa_circ_0000105 on NPC tumors.
Results
hsa_circ_0000105 and S100A11 were highly expressed in NPC, while miR-541-3p was lowly expressed. hsa_circ_0000105 competitively adsorbed miR-541-3p and mediated S100A11 expression. Silencing or upregulation of hsa_circ_0000105 restricts and induces malignant behavior in HNE2 cells, respectively. The impact of hsa_circ_0000105 silencing on malignant behaviors of HNE2 cells was blocked by miR-541-3p downregulation, while that of hsa_circ_0000105 upregulation was attenuated by S100A11 inhibition.
Conclusion
hsa_circ_0000105 acts as a carcinogenic factor in NPC and promotes NPC malignancy by miR-541-3p/S100A11 axis.
期刊介绍:
CLINICS is an electronic journal that publishes peer-reviewed articles in continuous flow, of interest to clinicians and researchers in the medical sciences. CLINICS complies with the policies of funding agencies which request or require deposition of the published articles that they fund into publicly available databases. CLINICS supports the position of the International Committee of Medical Journal Editors (ICMJE) on trial registration.