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ASS1 Overexpression: A Hallmark of Sonic Hedgehog Hepatocellular Adenomas; Recommendations for Clinical Practice.ASS1过表达： Sonic Hedgehog肝细胞腺瘤的一个标志；临床实践建议
Hepatol Commun. 2020 Apr 11;4(6):809-824. doi: 10.1002/hep4.1514. eCollection 2020 Jun.
2
Human Recombinant Arginase I [HuArgI (Co)-PEG5000]-Induced Arginine Depletion Inhibits Colorectal Cancer Cell Migration and Invasion.人重组精氨酸酶 I [HuArgI (Co)-PEG5000]诱导的精氨酸耗竭抑制结直肠癌细胞迁移和侵袭。
Int J Mol Sci. 2019 Nov 29;20(23):6018. doi: 10.3390/ijms20236018.
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Metabolic pathways of L-arginine and therapeutic consequences in tumors.L-精氨酸的代谢途径及其在肿瘤中的治疗后果。
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Nucleic Acids Res. 2019 Mar 18;47(5):2322-2335. doi: 10.1093/nar/gky1306.
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Mouse fetal intestinal organoids: new model to study epithelial maturation from suckling to weaning.鼠胎儿肠类器官：研究从哺乳期到离乳期上皮成熟的新模型。
EMBO Rep. 2019 Feb;20(2). doi: 10.15252/embr.201846221. Epub 2018 Dec 10.
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蜗牛通过抑制泛素化介导的 ASS1 降解来增强精氨酸的合成。

Snail enhances arginine synthesis by inhibiting ubiquitination-mediated degradation of ASS1.

机构信息

Tongren Hospital/Faculty of Basic Medicine, Hongqiao International Institute of Medicine, Shanghai Jiaotong University School of Medicine, Shanghai, China.

Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiaotong University School of Medicine, Shanghai, China.

出版信息

EMBO Rep. 2021 Aug 4;22(8):e51780. doi: 10.15252/embr.202051780. Epub 2021 Jun 29.

DOI:10.15252/embr.202051780
PMID:34184805
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8339691/
Abstract

Snail is a dedicated transcriptional repressor and acts as a master inducer of EMT and metastasis, yet the underlying signaling cascades triggered by Snail still remain elusive. Here, we report that Snail promotes colorectal cancer (CRC) migration by preventing non-coding RNA LOC113230-mediated degradation of argininosuccinate synthase 1 (ASS1). LOC113230 is a novel Snail target gene, and Snail binds to the functional E-boxes within its proximal promoter to repress its expression in response to TGF-β induction. Ectopic expression of LOC113230 potently suppresses CRC cell growth, migration, and lung metastasis in xenograft experiments. Mechanistically, LOC113230 acts as a scaffold to facilitate recruiting LRPPRC and the TRAF2 E3 ubiquitin ligase to ASS1, resulting in enhanced ubiquitination and degradation of ASS1 and decreased arginine synthesis. Moreover, elevated ASS1 expression is essential for CRC growth and migration. Collectively, these findings suggest that TGF-β and Snail promote arginine synthesis via inhibiting LOC113230-mediated LRPPRC/TRAF2/ASS1 complex assembly and this complex can serve as potential target for the development of new therapeutic approaches to treat CRC.

摘要

蜗牛是一种专门的转录抑制剂，作为 EMT 和转移的主要诱导剂，但其触发的潜在信号级联仍然难以捉摸。在这里，我们报告说，蜗牛通过防止非编码 RNA LOC113230 介导的精氨酸琥珀酸合成酶 1 (ASS1) 降解来促进结直肠癌 (CRC) 的迁移。LOC113230 是蜗牛的一个新靶基因，蜗牛结合其近端启动子中的功能性 E 盒，以响应 TGF-β 诱导来抑制其表达。LOC113230 的异位表达在异种移植实验中有力地抑制了 CRC 细胞的生长、迁移和肺转移。在机制上，LOC113230 作为一个支架，促进 LRPPRC 和 TRAF2 E3 泛素连接酶与 ASS1 的募集，导致 ASS1 的泛素化和降解增强，精氨酸合成减少。此外，ASS1 表达的升高对于 CRC 的生长和迁移是必不可少的。总之，这些发现表明 TGF-β 和蜗牛通过抑制 LOC113230 介导的 LRPPRC/TRAF2/ASS1 复合物组装来促进精氨酸合成，并且该复合物可以作为开发新的治疗方法治疗 CRC 的潜在靶点。