Esposito Jessica Elisabetta, De Iuliis Vincenzo, Avolio Francesco, Liberatoscioli Eliana, Pulcini Riccardo, Di Francesco Simona, Pennelli Alfonso, Martinotti Stefano, Toniato Elena
Center of Advanced Studies and Technology, Department of Innovative Technology in Medicine and Dentistry, University of Chieti, 66100 Chieti, Italy.
Department of Clinical Pathology, G. Mazzini Civil Hospital, ASL 4, 64100 Teramo, Italy.
Cancers (Basel). 2022 May 6;14(9):2309. doi: 10.3390/cancers14092309.
TRIM/RBCC are a large family of proteins that include more than 80 proteins, most of which act as E3 ligases and catalyze the direct transfer of Ubiquitin, SUMO and ISG15 on specific protein substrates. They are involved in oncogenesis processes and in cellular immunity. On this topic, we focus on TRIM8 and its multiple roles in tumor pathologies. TRIM8 inhibits breast cancer proliferation through the regulation of estrogen signaling. TRIM8 downregulation in glioma is involved in cell proliferation, and it is related to patients' survival. Several studies suggested that TRIM8 regulates the p53 suppressor signaling pathway: it is involved in the NF-kB pathway (Nuclear Factor kappa light- chain-enhancer of activated B cells) and in STAT3 (Signal Transducer and Activator of Transcription 3) of the JAK-STAT pathway. In this review, we summarize how the association between these different pathways reflects a dual role of TRIM8 in cancer as an oncogene or a tumor suppressor gene.
TRIM/RBCC是一个包含80多种蛋白质的大家族，其中大多数充当E3连接酶，并催化泛素、SUMO和ISG15在特定蛋白质底物上的直接转移。它们参与肿瘤发生过程和细胞免疫。关于这个主题，我们重点关注TRIM8及其在肿瘤病理学中的多种作用。TRIM8通过调节雌激素信号传导来抑制乳腺癌增殖。胶质瘤中TRIM8的下调与细胞增殖有关，并且与患者的生存率相关。多项研究表明，TRIM8调节p53抑制信号通路：它参与NF-kB通路（活化B细胞的核因子κ轻链增强子）和JAK-STAT通路中的STAT3（信号转导和转录激活因子3）。在这篇综述中，我们总结了这些不同通路之间的关联如何反映TRIM8在癌症中作为癌基因或肿瘤抑制基因的双重作用。
