中国口腔颌面外科杂志 ›› 2025, Vol. 23 ›› Issue (4): 331-339.doi: 10.19438/j.cjoms.2025.04.004

• 论著 • 上一篇    下一篇

USP20通过NF-κB信号通路对口腔鳞癌恶性生物学行为的影响及机制探讨

刘搏, 翟晓奇, 刘雨璐, 王思丹, 关键   

  1. 佳木斯大学附属口腔医院 口腔颌面外科,黑龙江 佳木斯 154000
  • 收稿日期:2025-01-16 修回日期:2025-04-01 出版日期:2025-07-20 发布日期:2025-08-04
  • 通讯作者: 关键,E-mail: guanjian1207@163.com
  • 作者简介:刘搏(1993-),男,硕士研究生,主治医师,E-mail: dr15542155805@163.com
  • 基金资助:
    黑龙江省卫生健康委科技计划(20240808020129)

The effect and mechanism of USP20 on the malignant biological behavior of oral squamous cell carcinoma through NF-κB signaling pathway

Liu Bo, Zhai Xiaoqi, Liu Yulu, Wang Sidan, Guan Jian   

  1. Department of Oral and Maxillofacial Surgery, The Affiliated Stomatological Hospital of Jiamusi University. Jiamusi 154000, Heilongjiang Province, China
  • Received:2025-01-16 Revised:2025-04-01 Online:2025-07-20 Published:2025-08-04

摘要: 目的:探讨泛素特异性蛋白酶20(ubiquitin specific protease 20, USP20)通过核因子-κB(nuclear factor-kappa B,NF-κB)信号通路对口腔鳞癌(oral squamous cell carcinoma, OSCC)恶性生物学行为的影响及机制。方法:通过生物信息学分析、蛋白免疫印迹实验、免疫组织化学染色等检测OSCC组织中USP20的表达,通过癌症基因组图谱(The Cancer Genome Atlas,TCGA)数据库分析USP20与OSCC临床病理指标的相关性。构建稳转敲低USP20的人舌鳞癌CAL-27细胞,通过体内和体外实验评价USP20对OSCC恶性生物学行为的影响。通过RNA高通量测序,结合测序结果及蛋白免疫印迹定量分析,探讨USP20影响OSCC病程的潜在机制。结果:USP20在OSCC组织中过表达。敲低USP20可抑制CAL-27的体外增殖、侵袭和迁移能力,抑制CAL-27细胞异种皮下移植瘤的生长。敲低USP20可抑制CAL-27细胞NF-κB信号通路,并抑制肿瘤细胞恶性行为的发生。结论:USP20在OSCC中过表达,并通过NF-κB信号通路促进口腔鳞癌的生长与转移。

关键词: USP20, 泛素特异性蛋白酶, 口腔鳞癌, CAL-27, NF-κB, 恶性生物学行为, 癌基因

Abstract: PURPOSE: To explore the effects and mechanisms of ubiquitin specific protease 20(USP20) on the malignant biological behavior of oral squamous cell carcinoma(OSCC) through the nuclear factor-kappa B(NF-κB) signaling pathway. METHODS: The expression of USP20 in OSCC tissues was studied by bioinformatics analysis, Western blot assay and immunohistochemical staining. The Cancer Genome Atlas(TCGA) database was used to explore the correlation between USP20 and OSCC clinicopathological indicators. Human tongue squamous cell carcinoma CAL-27 cells with stable and lower expression of USP20 were constructed to investigate the effect of USP20 on the malignant biological behavior of OSCC through in vivo and in vitro experiments. The potential mechanism of USP20 affecting OSCC was explored through high-throughput RNA sequencing, combined with quantitative analysis of sequencing results and protein Western blot. RESULTS: USP20 was overexpressed in OSCC tissues. Knockdown of USP20 inhibited the proliferation, invasion and migration of CAL-27 cells in vitro, and inhibited the growth of CAL-27 cell xenograft tumors. Knockdown of USP20 could inhibit the NF-κB signaling pathway in CAL-27 cells and inhibit the malignant behavior of tumor cells. CONCLUSIONS: USP20 is overexpressed in OSCC and promotes the growth and metastasis of OSCC through NF-κB signaling pathway.

Key words: USP20, Ubiquitin specific protease, Oral squamous cell carcinoma, CAL-27, NF-κB, malignant biological behavior, Oncogene

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