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三重基序家族蛋白(TRIMs)在乳腺癌中的新作用。

Emerging roles of tripartite motif family proteins (TRIMs) in breast cancer.

作者信息

Cao Jianing, Yang Mengdi, Guo Duancheng, Tao Zhonghua, Hu Xichun

机构信息

Department of Breast and Urologic Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.

Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.

出版信息

Cancer Med. 2024 Jul;13(14):e7472. doi: 10.1002/cam4.7472.

DOI:10.1002/cam4.7472
PMID:39016065
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11252664/
Abstract

Breast cancer (BC) is the most common malignant tumor worldwide. Despite enormous progress made in the past decades, the underlying mechanisms of BC remain further illustrated. Recently, TRIM family proteins proved to be engaged in BC progression through regulating various aspects. Here we reviewed the structures and basic functions of TRIM family members and first classified them into three groups according to canonical polyubiquitination forms that they could mediate: K48- only, K63- only, and both K48- and K63-linked ubiquitination. Afterwards, we focused on the specific biological functions and mechanisms of TRIMs in BCs, including tumorigenesis and invasiveness, drug sensitivity, tumor immune microenvironment (TIME), cell cycle, and metabolic reprogramming. We also explored the potential of TRIMs as novel biomarkers for predicting prognosis and future therapeutic targets in BC.

摘要

乳腺癌(BC)是全球最常见的恶性肿瘤。尽管在过去几十年中取得了巨大进展,但BC的潜在机制仍有待进一步阐明。最近,TRIM家族蛋白被证明通过调节多个方面参与BC的进展。在此,我们综述了TRIM家族成员的结构和基本功能,并首先根据它们能够介导的典型多聚泛素化形式将其分为三组:仅K48连接、仅K63连接以及K48和K63连接的泛素化。之后,我们重点关注了TRIMs在BC中的特定生物学功能和机制,包括肿瘤发生和侵袭性、药物敏感性、肿瘤免疫微环境(TIME)、细胞周期和代谢重编程。我们还探讨了TRIMs作为预测BC预后的新型生物标志物和未来治疗靶点的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c250/11252664/b1879e4b4cf4/CAM4-13-e7472-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c250/11252664/647c00573c06/CAM4-13-e7472-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c250/11252664/58dda98416bb/CAM4-13-e7472-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c250/11252664/b1879e4b4cf4/CAM4-13-e7472-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c250/11252664/647c00573c06/CAM4-13-e7472-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c250/11252664/58dda98416bb/CAM4-13-e7472-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c250/11252664/b1879e4b4cf4/CAM4-13-e7472-g003.jpg

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1
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本文引用的文献

1
An E3 ligase TRIM1 promotes colorectal cancer progression via K63-linked ubiquitination and activation of HIF1α.一种E3泛素连接酶TRIM1通过K63连接的泛素化和HIF1α的激活促进结直肠癌进展。
Oncogenesis. 2024 May 20;13(1):16. doi: 10.1038/s41389-024-00517-2.
2
The E3 ubiquitin ligase TRIM39 modulates renal fibrosis induced by unilateral ureteral obstruction through regulating proteasomal degradation of PRDX3.E3泛素连接酶TRIM39通过调节PRDX3的蛋白酶体降解来调控单侧输尿管梗阻诱导的肾纤维化。
Cell Death Discov. 2024 Jan 9;10(1):17. doi: 10.1038/s41420-023-01785-4.
3
Nuclear cGAS restricts L1 retrotransposition by promoting TRIM41-mediated ORF2p ubiquitination and degradation.
核 cGAS 通过促进 TRIM41 介导的 ORF2p 泛素化和降解来限制 L1 retrotransposition。
Nat Commun. 2023 Dec 12;14(1):8217. doi: 10.1038/s41467-023-43001-y.
4
TRIM45 aggravates microglia pyroptosis via Atg5/NLRP3 axis in septic encephalopathy.TRIM45 通过 Atg5/NLRP3 轴加重脓毒症性脑病中的小胶质细胞焦亡。
J Neuroinflammation. 2023 Nov 30;20(1):284. doi: 10.1186/s12974-023-02959-8.
5
TRIM29 promotes antitumor immunity through enhancing IGF2BP1 ubiquitination and subsequent PD-L1 downregulation in gastric cancer.TRIM29 通过增强 IGF2BP1 的泛素化及随后下调 PD-L1 促进胃癌中的抗肿瘤免疫。
Cancer Lett. 2024 Jan 28;581:216510. doi: 10.1016/j.canlet.2023.216510. Epub 2023 Nov 27.
6
Investigation into the role of the MITA-TRIM38 interaction in regulating pyroptosis and maintaining immune tolerance at the maternal-fetal interface.探讨 MITA-TRIM38 相互作用在调节母胎界面细胞焦亡和维持免疫耐受中的作用。
Cell Death Dis. 2023 Nov 28;14(11):780. doi: 10.1038/s41419-023-06314-w.
7
E3 ligase Trim35 inhibits LSD1 demethylase activity through K63-linked ubiquitination and enhances anti-tumor immunity in NSCLC.E3 连接酶 Trim35 通过 K63 连接的泛素化抑制 LSD1 去甲基酶活性,并增强 NSCLC 中的抗肿瘤免疫。
Cell Rep. 2023 Dec 26;42(12):113477. doi: 10.1016/j.celrep.2023.113477. Epub 2023 Nov 20.
8
TRIM3 facilitates ferroptosis in non-small cell lung cancer through promoting SLC7A11/xCT K11-linked ubiquitination and degradation.TRIM3 通过促进 SLC7A11/xCT K11 链接泛素化和降解促进非小细胞肺癌中的铁死亡。
Cell Death Differ. 2024 Jan;31(1):53-64. doi: 10.1038/s41418-023-01239-5. Epub 2023 Nov 17.
9
FOXA2 Suppression by TRIM36 Exerts Anti-Tumor Role in Colorectal Cancer Via Inducing NRF2/GPX4-Regulated Ferroptosis.FOXA2 通过抑制 TRIM36 在结直肠癌中发挥抑瘤作用,通过诱导 NRF2/GPX4 调节的铁死亡。
Adv Sci (Weinh). 2023 Dec;10(35):e2304521. doi: 10.1002/advs.202304521. Epub 2023 Oct 24.
10
The E3 ligase TRIM26 suppresses ferroptosis through catalyzing K63-linked ubiquitination of GPX4 in glioma.E3 连接酶 TRIM26 通过催化 GPX4 的 K63 链接泛素化来抑制脑胶质瘤中的铁死亡。
Cell Death Dis. 2023 Oct 23;14(10):695. doi: 10.1038/s41419-023-06222-z.