Huang Yu-Hao, Chien Peng-Ju, Wang Wen-Ling, Hsu Li-Sung, Huang Yen-Min, Chang Wen-Wei
Department of Biomedical Sciences, Chung Shan Medical University, Taichung 402306, Taiwan, R.O.C.
Institute of Medicine, Chung Shan Medical University, Taichung 402306, Taiwan, R.O.C.
Int J Mol Med. 2025 Mar;55(3). doi: 10.3892/ijmm.2025.5485. Epub 2025 Jan 10.
Oral squamous cell carcinoma (OSCC) is a type of head and neck cancer (HNC) with a high recurrence rate, which has been reported to be associated with the presence of cancer stem cells (CSCs). Tribbles pseudokinase 3 (TRIB3) is involved in intracellular signaling and the aim of the present study was to investigate the role of TRIB3 in the maintenance of CSCs. Analysis of The Cancer Genome Atlas database samples demonstrated a positive correlation between TRIB3 expression levels and shorter overall survival rates in patients with HNC. Knockdown of TRIB3 in the SAS and HSC-3 OSCC cell lines reduced cell proliferation through the induction of cell cycle arrest, but not of apoptosis. The population of OSCC-CSCs, defined by a high level of intracellular aldehyde dehydrogenase activity and the ability to form tumorspheres, was also reduced in TRIB3-silenced OSCC cells. The tumorigenicity of tumorspheres derived from the SAS OSCC cell line was reduced following TRIB3 knockdown. These results suggested the potential involvement of TRIB3 in the self-renewal capability of the OSCC CSCs. Mechanistically, TRIB3 was shown to positively regulate SOX2 expression via maintaining both the protein expression level and the SOX2 promoter-binding capability of E2F transcription factor 1 (E2F1). Additionally, TRIB3 also increased the expression level of EGFR through preventing its lysosomal degradation. The significant associations between TRIB3 and E2F1, SOX2 or EGFR expression were also confirmed using a HNC tissue array. Taken together, the findings of the present study may suggest that TRIB3 is an oncogenic protein that supports the stemness of OSCC and that targeting TRIB3 may be a potential strategy for OSCC therapy in the future.
口腔鳞状细胞癌(OSCC)是一种头颈部癌症(HNC),复发率很高,据报道与癌症干细胞(CSC)的存在有关。Tribbles假激酶3(TRIB3)参与细胞内信号传导,本研究的目的是探讨TRIB3在CSC维持中的作用。对癌症基因组图谱数据库样本的分析表明,HNC患者中TRIB3表达水平与较短的总生存率之间存在正相关。在SAS和HSC-3 OSCC细胞系中敲低TRIB3可通过诱导细胞周期停滞而非细胞凋亡来降低细胞增殖。由高水平的细胞内醛脱氢酶活性和形成肿瘤球的能力所定义的OSCC-CSC群体,在TRIB3沉默的OSCC细胞中也减少了。TRIB3敲低后,源自SAS OSCC细胞系的肿瘤球的致瘤性降低。这些结果表明TRIB3可能参与了OSCC CSC的自我更新能力。机制上,TRIB3通过维持E2F转录因子1(E2F1)的蛋白质表达水平和SOX2启动子结合能力,被证明可正向调节SOX2表达。此外,TRIB3还通过防止表皮生长因子受体(EGFR)的溶酶体降解来增加其表达水平。使用HNC组织芯片也证实了TRIB3与E2F1、SOX2或EGFR表达之间的显著关联。综上所述,本研究的结果可能表明TRIB3是一种支持OSCC干性的致癌蛋白,靶向TRIB3可能是未来OSCC治疗的一种潜在策略。