[摘 要] 目的：探究环状RNA hsa_circ_0081621对人喉鳞状细胞癌AMC-HN-8和TU177细胞恶性生物学行为的影响。方法：常规培养AMC-HN-8和TU177细胞，用转染试剂将si-NC、si-hsa_circ_0081621、空载体（vector）和hsa_circ_0081621过表达载体（hsa_circ_0081621-OE）转染至AMC-HN-8和TU177细胞，分别记作si-NC、si-hsa_circ_0081621、vector和hsa_circ_0081621-OE组。用CCK-8法、克隆形成实验、划痕愈合实验和Transwell小室实验分别检测敲减或过表达hsa_circ_0081621对AMC-HN-8和TU177细胞增殖、迁移和侵袭能力的影响。结果：在AMC-HN-8和TU177中成功地敲减或过表达了hsa_circ_0081621；敲减或过表达hsa_circ_0081621能显著抑制或促进AMC-HN-8和TU177细胞的增殖、迁移和侵袭能力（P < 0.01或P < 0.001或P < 0.000 1）。结论：hsa_circ_0081621可促进人喉鳞状细胞癌AMC-HN-8和TU177细胞的恶性生物学行为。

[摘 要] 目的：本研究旨在探讨转录因子HOXC13在喉鳞状细胞癌（LSCC）中的表达、功能及可能的调控机制。方法：常规培养LSCC细胞，将其分为sh-NC组、sh-HOXC13组、pcDNA3.1-NC组、pcDNA3.1-HOXC13组、pcDNA3.1-PCNA组和sh-HOXC13+pcDNA3.1-PCNA组，用转染试剂将相应核酸和质粒转染各组细胞。用数据库数据分析HOXC13 mRNA在LSCC组织中的表达；收集2019年1月至2022年12月在联勤保障部队第九八〇医院耳鼻咽喉头颈外科手术切除的62对LSCC组织及配对的癌旁组织，免疫组织化学法检测中国人LSCC组织中HOXC13蛋白的表达，qPCR检测中国人LSCC组织、癌旁组织以及各组细胞中HOXC13和PCNA mRNA的表达，MTS法检测各组AMC-HN-8细胞的增殖能力，平板克隆实验检测各组AMC-HN-8细胞的克隆形成能力，Transwell小室实验检测各组AMC-HN-8细胞的迁移和侵袭能力，双萤光素酶报告基因实验和染色质免疫沉淀技术（ChIP）验证HOXC13与PCNA之间的结合关系。结果：HOXC13和PCNA在LSCC组织和细胞中均呈高表达（P<0.05或P<0.01）且两者的表达水平呈正相关（P<0.01），HOXC13的表达水平与TNM分期有明显关联（P<0.01）。敲减HOXC13可明显抑制AMC-HN-8细胞的增殖、迁移和侵袭能力（均P<0.01），过表达HOXC13则促进TU686细胞的增殖、迁移和侵袭能力（均P<0.01）。HOXC13可与PCNA启动子区结合并调控其转录。敲低PCNA可部分逆转HOXC13对AMC-HN-8细胞的恶性生物学行为的促进作用（均P<0.01）。结论：HOXC13通过上调PCNA促进LSCC细胞的恶性生物学行为，HOXC13是LSSC临床诊断和治疗的潜在靶点。

【Objective】To investigate the effect of miR- 127-3p on proliferation，apoptosis，migration and invasion of uveal melanoma cells.【Methods】The expression of miR- 127- 3p and MAPK4 mRNA in human uveal melanoma tissues and cells，normal tissues and cells were detected by RT-qPCR. The mimic-NC，miR-127-3p mimic，pc-MAPK4 plasmids were transfected into SP6.5 or OM431 cells，respectively，by Lipofectamine 2000. The relationship between miR-127-3p and MAPK4 counterstaining was detected by dual luciferase assay. Cell proliferation was detected by CCK- 8 method，apoptosis was detected by flow cytometry，cell migration ability was detected by scratch test，cell invasion ability was detected by Transwell method，and relative expression level of AKT/mTOR pathway protein was detected by Western blot.【Results】In uveal melanoma tissues and cell lines，the expression of miR- 127-3p was down-regulated（P < 0.01）while that of MAPK4 expression was significantly up-regulated（P < 0.01）. The binding site of miR-127-3p and MAPK4 3′UTR region，the high expression of miR-127-3p significantly inhibited the luciferase activity of wild-type MAPK4 plasmid（P < 0.01），but the mutant MAPK4 plasmid Luciferase activity has no effect. Compared with the Control group ，the proliferation of SP6.5 cells and OM431 cells in miR- 127-3p mimic group were significantly decreased（P < 0.01），and the apoptotic rate was significantly increased（P < 0.01）. The scratch closure rate was obvious. The decrease（P < 0.01）， the number of invading cells per field was significantly decreased（P < 0.01），and the expression of p-AKT（T308）/AKT and p-mTORr（S473）/mTOR protein were significantly down-regulated（P < 0.01）. Transfection of pc-MAPK4 reversed the above changes.【Conclusion】MiR-127-3p inhibits proliferation，migration and invasion of uveal melanoma cells and induces apoptosis by down-regulating MAPK4，which may be involved in the inhibition of AKT/mTOR pathway activation.