Jiang Liangqian, Mu Haiyu, Xing Huixia, Zhu Feng, Zhao Xiangyu, Wu Yongxia
Department of Laboratory Medicine, Linyi Peoples' Hospital, Linyi, Shandong, China.
School of Public Health, Suzhou Vocational Health College, Suzhou, Jiangsu, China.
Int J Biol Macromol. 2025 Sep;321(Pt 1):146194. doi: 10.1016/j.ijbiomac.2025.146194. Epub 2025 Jul 21.
The ubiquitin-proteasome pathway is a critical regulatory system in eukaryotic cells, which mediates dynamic and reversible protein modifications through the E1-E2-E3 ubiquitination cascade. E3 ubiquitin ligases, which catalyze substrate-specific ubiquitination for proteasomal degradation, play essential roles in maintaining cellular homeostasis. The deltex E3 ubiquitin ligase 3 L (DTX3L) modulates a variety of biological processes, such as proliferation, cell cycle, migration, invasion and apoptosis. Emerging evidence implicates DTX3L dysregulation in the pathogenesis of multiple malignancies, including cervical cancer, melanoma, prostate cancer, triple-negative breast cancer, glioma and pancreatic cancer. This review synthesizes current knowledge on DTX3L's molecular mechanisms across tumor types, highlighting its role in modulating the stability of oncogenic and tumor-suppressive substrates. As DTX3L emerges as a promising oncology therapeutic target, its molecular functions and regulatory mechanisms offers novel opportunities for rational antitumor drug design. However, the clinical translatability of DTX3L-targeted strategies requires further validation. In conclusion, DTX3L has the potential to serve as a novel cancer biomarker and therapeutic target.
泛素-蛋白酶体途径是真核细胞中的一个关键调节系统,它通过E1-E2-E3泛素化级联反应介导动态且可逆的蛋白质修饰。E3泛素连接酶催化底物特异性泛素化以进行蛋白酶体降解,在维持细胞稳态中发挥着重要作用。德尔塔E3泛素连接酶3L(DTX3L)调节多种生物学过程,如增殖、细胞周期、迁移、侵袭和凋亡。新出现的证据表明DTX3L失调与多种恶性肿瘤的发病机制有关,包括宫颈癌、黑色素瘤、前列腺癌、三阴性乳腺癌、神经胶质瘤和胰腺癌。本综述综合了目前关于DTX3L在不同肿瘤类型中的分子机制的知识,突出了其在调节致癌和抑癌底物稳定性方面的作用。由于DTX3L已成为一个有前景的肿瘤治疗靶点,其分子功能和调节机制为合理的抗肿瘤药物设计提供了新的机会。然而,针对DTX3L的策略的临床可转化性需要进一步验证。总之,DTX3L有潜力作为一种新型癌症生物标志物和治疗靶点。