[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。

[Abstract] Objective:To detect the expression of transcription factor FOXP4 (Forkhead box P4) in laryngeal squamous cell carcinoma (LSCC) tissues and cell lines, and to investigate its effects on the proliferation, migration, invasion, cell cycle, and apoptosis of LSCC TU177 cells in vitro as well as to explore its relationship with epithelial-mesenchymal transition (EMT) process. Methods: A total of 40 pairs of tumor tissues and adjacent tissues that resected from LSCC patients were collected from the biological specimen bank of the Forth Hospital of Hebei Medical University between 2013 and 2015. The expression of FOXP4 in LSCC tissues and corresponding adjacent tissues was detected by qPCR. qPCR and Western blotting were used to detect the FOXP4 expression level in human LSCC cell lines (AMC-HN-8, TU177, TU686, and TU212). Small interfering RNA (si-RNA) was used to knock down FOXP4 expression in TU177 cells. The effects of FOXP4 knockdown on the proliferation, migration, invasion, cell cycle and apoptosis of TU177 cells were measured by MTS assay, clone formation assay, Transwell chamber migration and invasion assay, and flow cytometry, respectively. The mRNA levels of EMT markers N-cadherin, β-catenin, Vimentin, Twist, Snail and zine finger E box binding homeobox 1 (ZEB1) after transfection of si-FOXP4 in TU177 cells were detected by qPCR. The changes of protein levels of N-cadherin, β-catenin, Vimentin and Twist after FOXP4 knockdown were measured by Western blotting. Results: The expression of FOXP4 in LSCC tissues was significantly higher than that in adjacent tissues (P<0.05), and it was related to the TNM stage of tumors and lymph node metastasis (all P<0.05). The expression of FOXP4 in LSCC cells was higher than that in the adjacent tissues (P<0.05 or P<0.01). The expression of FOXP4 in TU177 cells transfected with si-FOXP4 was significantly lower than that in the control group (P<0.01). Compared with the control group, knocking down FOXP4 could inhibit the proliferation, migration and invasion but promote the apoptosis of TU177 cells in vitro (all P<0.01), block the cell cycle at G0/G1 phase (P<0.01), and reduce cell replication in S phase (P<0.01); in addition, knocking down FOXP4 could reduce the mRNA levels of N-cadherin, β-catenin, Vimentin, Twist, Snail, ZEB1 (P<0.05 or P<0.01) and the protein levels of N-cadherin, β-catenin, Vimentin, Twist in TU177 cells. Conclusion: The high expression of FOXP4 may be related to the occurrence and development of LSCC. FOXP4 knockdown can inhibit the proliferation, migration and invasion of laryngeal cancer cells in vitro, block cell cycle at G0/G1 phase, promote apoptosis, and may participate in the EMT process.