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E3泛素连接酶BTBD3通过调节TYRO3/ Wnt/β-连环蛋白信号轴抑制结直肠癌的肿瘤发生。

E3 ubiquitin ligase BTBD3 inhibits tumorigenesis of colorectal cancer by regulating the TYRO3/Wnt/β-catenin signaling axis.

作者信息

Ye Kai, Wang Peng-Cheng, Chen Yan-Xin, Huang Qiao-Zhen, Chi Pan

机构信息

Department of Colorectal Surgery, Fujian Medical University Union Hospital, Fuzhou, 350001, China.

Department of Surgery, The Second Affiliated Hospital, Fujian Medical University, Quanzhou, Fujian Province, 362000, China.

出版信息

Cancer Cell Int. 2024 Sep 3;24(1):306. doi: 10.1186/s12935-024-03478-z.

DOI:10.1186/s12935-024-03478-z
PMID:39227913
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11373184/
Abstract

Clinical trials and studies have implicated that E3 ubiquitin ligase BTBD3 (BTB Domain Containing 3) is a cancer-associated gene. However, the role and underlying mechanism of BTBD3 in colorectal cancer (CRC) is not fully understood yet. Herein, our study demonstrated that the mRNA and protein levels of BTBD3 were decreased in CRC tissues and associated with TYPO3 and Wnt/β-catenin pathway. Our results showed that circRAE1 knockdown and TYRO3 overexpression activated Wnt/β-catenin signaling pathway and the EMT process-associated markers, indicating that circRAE1/miR-388-3p/TYRO3 axis exacerbated tumorigenesis of CRC by activating Wnt/β-catenin signaling pathway. In addition, overexpression of BTBD3 reduced CRC cell migration and invasion in vitro and inhibited tumor growth in vivo. Our data demonstrated that BTBD3 suppressed CRC progression through negative regulation of the circRAE1/miR-388-3p/TYRO3 axis and the Wnt/β-catenin pathway. Our data further confirmed that BTBD3 bound and ubiquitinated β-catenin and led to β-catenin degradation, therefore blocked the Wnt/β-catenin pathway and suppressed the CRC tumorigenesis. This study explored the mechanism of BTBD3 involved in CRC tumorigenesis and provided a new theoretical basis for the prevention and treatment of CRC.

摘要

临床试验和研究表明，E3泛素连接酶BTBD3（含BTB结构域蛋白3）是一种癌症相关基因。然而，BTBD3在结直肠癌（CRC）中的作用及潜在机制尚未完全明确。在本研究中，我们发现CRC组织中BTBD3的mRNA和蛋白水平降低，且与TYPO3及Wnt/β-连环蛋白信号通路相关。我们的结果显示，circRAE1敲低和TYRO3过表达激活了Wnt/β-连环蛋白信号通路以及与上皮-间质转化（EMT）过程相关的标志物，这表明circRAE1/miR-388-3p/TYRO3轴通过激活Wnt/β-连环蛋白信号通路加剧了CRC的肿瘤发生。此外，BTBD3过表达在体外降低了CRC细胞的迁移和侵袭能力，并在体内抑制了肿瘤生长。我们的数据表明，BTBD3通过对circRAE1/miR-388-3p/TYRO3轴和Wnt/β-连环蛋白信号通路的负调控来抑制CRC进展。我们的数据进一步证实，BTBD3与β-连环蛋白结合并使其泛素化，导致β-连环蛋白降解，从而阻断Wnt/β-连环蛋白信号通路并抑制CRC的肿瘤发生。本研究探索了BTBD3参与CRC肿瘤发生的机制，为CRC的防治提供了新的理论依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/939d/11373184/b3df989933de/12935_2024_3478_Fig5_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/939d/11373184/bd5bec021254/12935_2024_3478_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/939d/11373184/b3df989933de/12935_2024_3478_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/939d/11373184/6a827bce6d22/12935_2024_3478_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/939d/11373184/484a68c41fec/12935_2024_3478_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/939d/11373184/b343a303e801/12935_2024_3478_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/939d/11373184/7a158ab5cb7f/12935_2024_3478_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/939d/11373184/13f13d7bc85c/12935_2024_3478_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/939d/11373184/ceee3faaf437/12935_2024_3478_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/939d/11373184/bd5bec021254/12935_2024_3478_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/939d/11373184/b3df989933de/12935_2024_3478_Fig5_HTML.jpg

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