脱氮酶
头颈部鳞状细胞癌
转移
癌症研究
泛素
泛素连接酶
头颈部
细胞
生物
头颈部癌
上皮-间质转换
细胞培养
癌症
化学
癌症干细胞
下调和上调
干细胞
医学
基因敲除
抗药性
细胞生长
基底细胞
癌细胞
鳞癌
抑制器
作者
Xueying Wang,Yang Zhou,Jiaqi Tan,Diekuo Zhang,Chao Liu,Juncheng Wang,Xin Zhang,Gangcai Zhu,Yong Liu
标识
DOI:10.1073/pnas.2504068123
摘要
The development of metastasis marks an aggressive stage of head and neck squamous cell carcinoma (HNSCC) and is closely linked to unfavorable survival outcomes. While metadherin (MTDH) drives tumorigenesis, metastasis, and chemoresistance in HNSCC, its dysregulation mechanisms remain unclear. Here, we identify USP14 as a specific deubiquitinase that stabilizes MTDH. USP14-dependent deubiquitination of MTDH activates NF-κB signaling, which drives epithelial-mesenchymal transition and supports cancer stem cells maintenance, ultimately strengthening HNSCC metastasis and chemoresistance. Mechanistically, we uncovered a competitive interaction: USP14 competes with the ubiquitin ligase FBXW7 for MTDH binding, preventing FBXW7-mediated degradation. Consequently, USP14 inhibition significantly mitigates aggressive phenotypes, an effect reversed by MTDH reintroduction. Clinical analysis confirms that MTDH and USP14 are overexpressed and positively correlated in metastatic HNSCC tissues. In conclusion, our study reveals a regulatory axis where USP14 competitively counteracts FBXW7 to stabilize MTDH, driving HNSCC progression. These findings provide preclinical evidence that targeting USP14 is a promising therapeutic strategy to overcome metastasis and chemoresistance in HNSCC.
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