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翻译后修饰在结直肠癌转移中的作用

Role of Post-Translational Modifications in Colorectal Cancer Metastasis.

作者信息

Peng Na, Liu Jingwei, Hai Shuangshuang, Liu Yihong, Zhao Haibo, Liu Weixin

机构信息

Department of Gastroenterology, The First Affiliated Hospital of China Medical University, Shenyang 110001, China.

Department of Anus and Intestine Surgery, The First Affiliated Hospital of China Medical University, Shenyang 110001, China.

出版信息

Cancers (Basel). 2024 Feb 3;16(3):652. doi: 10.3390/cancers16030652.

DOI:10.3390/cancers16030652
PMID:38339403
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10854713/
Abstract

Colorectal cancer (CRC) is one of the most common malignant tumors of the digestive tract. CRC metastasis is a multi-step process with various factors involved, including genetic and epigenetic regulations, which turn out to be a serious threat to CRC patients. Post-translational modifications (PTMs) of proteins involve the addition of chemical groups, sugars, or proteins to specific residues, which fine-tunes a protein's stability, localization, or interactions to orchestrate complicated biological processes. An increasing number of recent studies suggest that dysregulation of PTMs, such as phosphorylation, ubiquitination, and glycosylation, play pivotal roles in the CRC metastasis cascade. Here, we summarized recent advances in the role of post-translational modifications in diverse aspects of CRC metastasis and its detailed molecular mechanisms. Moreover, advances in drugs targeting PTMs and their cooperation with other anti-cancer drugs, which might provide novel targets for CRC treatment and improve therapeutic efficacy, were also discussed.

摘要

结直肠癌(CRC)是消化道最常见的恶性肿瘤之一。CRC转移是一个涉及多种因素的多步骤过程,包括遗传和表观遗传调控,这对CRC患者构成了严重威胁。蛋白质的翻译后修饰(PTM)涉及向特定残基添加化学基团、糖类或蛋白质,从而微调蛋白质的稳定性、定位或相互作用,以协调复杂的生物学过程。最近越来越多的研究表明,PTM的失调,如磷酸化、泛素化和糖基化,在CRC转移级联反应中起关键作用。在这里,我们总结了翻译后修饰在CRC转移各个方面的作用及其详细分子机制的最新进展。此外,还讨论了靶向PTM的药物进展及其与其他抗癌药物的协同作用,这可能为CRC治疗提供新的靶点并提高治疗效果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e50/10854713/5c63b79d9bb5/cancers-16-00652-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e50/10854713/d4f6322b90f2/cancers-16-00652-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e50/10854713/487a74802ab2/cancers-16-00652-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e50/10854713/fb09651e31ab/cancers-16-00652-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e50/10854713/a8bc8b702cbc/cancers-16-00652-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e50/10854713/8e5057c72d84/cancers-16-00652-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e50/10854713/5c63b79d9bb5/cancers-16-00652-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e50/10854713/d4f6322b90f2/cancers-16-00652-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e50/10854713/487a74802ab2/cancers-16-00652-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e50/10854713/fb09651e31ab/cancers-16-00652-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e50/10854713/a8bc8b702cbc/cancers-16-00652-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e50/10854713/8e5057c72d84/cancers-16-00652-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e50/10854713/5c63b79d9bb5/cancers-16-00652-g006.jpg

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Elucidation of E3 ubiquitin ligase specificity through proteome-wide internal degron mapping.通过全蛋白质组内部降解信号区域作图阐明 E3 泛素连接酶的特异性。
Mol Cell. 2023 Sep 21;83(18):3377-3392.e6. doi: 10.1016/j.molcel.2023.08.022.
2
Phosphorylation at tyrosine 317 and 508 are crucial for PIK3CA/p110α to promote CRC tumorigenesis.酪氨酸317和508位点的磷酸化对于PIK3CA/p110α促进结直肠癌肿瘤发生至关重要。
Cell Biosci. 2023 Sep 9;13(1):164. doi: 10.1186/s13578-023-01102-7.
3
Pan-cancer analysis of post-translational modifications reveals shared patterns of protein regulation.
翻译后修饰的泛癌分析揭示了蛋白质调控的共同模式。
Cell. 2023 Aug 31;186(18):3945-3967.e26. doi: 10.1016/j.cell.2023.07.013. Epub 2023 Aug 14.
4
Pharmacological targeting of Axin2 suppresses cell growth and metastasis in colorectal cancer.靶向 Axin2 的药理学治疗抑制结直肠癌中的细胞生长和转移。
Br J Pharmacol. 2023 Dec;180(23):3071-3091. doi: 10.1111/bph.16193. Epub 2023 Aug 18.
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CCDC85C suppresses colorectal cancer cells proliferation and metastasis through activating GSK-3β and promoting β-catenin degradation.CCDC85C通过激活GSK-3β并促进β-连环蛋白降解来抑制结肠癌细胞的增殖和转移。
Cell Signal. 2023 Sep;109:110799. doi: 10.1016/j.cellsig.2023.110799. Epub 2023 Jul 9.
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J Transl Med. 2023 Jun 27;21(1):418. doi: 10.1186/s12967-023-04267-4.
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