Hsa_circ_0000105通过miR-541-3p/S100A11轴促进鼻咽癌的恶性发展。
Hsa_circ_0000105 promotes nasopharyngeal carcinoma malignancy by miR-541-3p/S100A11 axis.
作者信息
Peng LuXing, Qin Jian, Qing DeFeng, Huang XinJun, Huang XiuRong
机构信息
Department of Clinical Oncology Center, Radiotherapy Ward 3, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning City, Guangxi Zhuang Autonomous Region, China.
Department of Clinical Oncology Center, Radiotherapy Ward 3, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning City, Guangxi Zhuang Autonomous Region, China.
出版信息
Clinics (Sao Paulo). 2025 Jan 28;80:100577. doi: 10.1016/j.clinsp.2025.100577. eCollection 2025.
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.
目的
本研究旨在探讨hsa_circ_0000105是否参与调控鼻咽癌（NPC）生物学行为的过程，并揭示其分子机制。
方法
收集NPC组织和正常组织，获取NPC细胞系和正常对照细胞系。通过RT-qPCR或蛋白质免疫印迹法评估hsa_circ_0000105/miR-541-3p/S100A11。采用CCK-8法、EdU法、Transwell法、伤口愈合法、流式细胞术和蛋白质免疫印迹法评估NPC细胞的生物学行为。应用双荧光素酶报告基因检测法和RNA免疫沉淀法评估hsa_circ_0000105/miR-541-3p/S100A11的直接靶向关系。实施肿瘤异种移植实验以评估hsa_circ_0000105对NPC肿瘤的影响。
结果
hsa_circ_0000105和S100A11在NPC中高表达，而miR-541-3p低表达。hsa_circ_0000105竞争性吸附miR-541-3p并介导S100A11表达。hsa_circ_0000105的沉默或上调分别限制和诱导HNE2细胞的恶性行为。miR-541-3p下调可阻断hsa_circ_0000105沉默对HNE2细胞恶性行为的影响，而S100A11抑制可减弱hsa_circ_0000105上调的影响。
结论
hsa_circ_0000105在NPC中作为致癌因子，通过miR-541-3p/SI00A11轴促进NPC的恶性发展。
Zotero 插件