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评估乳腺癌中 TRIP13 水平及潜在分子途径的研究

Evaluation of the TRIP13 level in breast cancer and insights into potential molecular pathways.

机构信息

Department of General Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.

Department of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.

出版信息

J Cell Mol Med. 2022 May;26(9):2673-2685. doi: 10.1111/jcmm.17278. Epub 2022 Mar 23.

DOI:10.1111/jcmm.17278
PMID:35322916
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9077308/
Abstract

TRIP13 is a member of the large superfamily of the AAA + ATPase proteins and is associated with a variety of activities. Emerging evidence has shown that TRIP13 may serve as an oncogene. However, the function of TRIP13 in breast cancer (BC) has not yet been elucidated. Here, a variety of bioinformatic tools and laboratory experiments were combined to analyse the expression patterns, prognostic value and functional network of TRIP13 in BC. Multiple databases and immunohistochemistry (IHC) indicated a higher TRIP13 expression in BC tissue compared with normal tissue. TRIP13 was highly expressed in lung metastatic lesions compared with primary tumours in a 4T1 cell implantation BALB/c mouse model of BC. Kaplan-Meier plots also revealed that high TRIP13 expression correlated with poor survival in patients with BC. Furthermore, gene set enrichment analysis revealed that TRIP13 was primarily enriched in the signalling pathway of PI3K-AKT-mTOR. Suppressing TRIP13 could inhibit the expression of related genes, as well as the proliferation and migration of BC cell. Finally, 10 hub genes with a high score of connectivity were filtered from the protein-protein interaction (PPI) network, including MAD2L1, CDC20, CDC5L, CDK1, CCNA2, BUB1B, RAD51, SPO11, KIF11 and AURKB. Thus, TRIP13 may be a promising prognostic biomarker and an effective therapeutic target for BC.

摘要

TRIP13 是 AAA+ATP 酶蛋白大家族的成员之一，与多种活性相关。新出现的证据表明，TRIP13 可能作为一种癌基因。然而，TRIP13 在乳腺癌（BC）中的功能尚未阐明。在这里，我们结合了多种生物信息学工具和实验室实验来分析 TRIP13 在 BC 中的表达模式、预后价值和功能网络。多个数据库和免疫组织化学（IHC）表明，与正常组织相比，BC 组织中 TRIP13 的表达更高。在 BC 的 4T1 细胞植入 BALB/c 小鼠模型中，与原发性肿瘤相比，肺转移病灶中 TRIP13 的表达更高。Kaplan-Meier 图还表明，高 TRIP13 表达与 BC 患者的不良生存相关。此外，基因集富集分析表明，TRIP13 主要富集在 PI3K-AKT-mTOR 信号通路中。抑制 TRIP13 可以抑制相关基因的表达，以及 BC 细胞的增殖和迁移。最后，从蛋白质-蛋白质相互作用（PPI）网络中筛选出了 10 个具有高连接得分的 hub 基因，包括 MAD2L1、CDC20、CDC5L、CDK1、CCNA2、BUB1B、RAD51、SPO11、KIF11 和 AURKB。因此，TRIP13 可能是一种有前途的预后生物标志物和 BC 的有效治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/256b/9077308/c468dad0cae5/JCMM-26-2673-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/256b/9077308/1627f533f4a0/JCMM-26-2673-g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/256b/9077308/a075ae89fae3/JCMM-26-2673-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/256b/9077308/daf1b078090c/JCMM-26-2673-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/256b/9077308/86d8273ebce4/JCMM-26-2673-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/256b/9077308/ddb38f5889eb/JCMM-26-2673-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/256b/9077308/c468dad0cae5/JCMM-26-2673-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/256b/9077308/1627f533f4a0/JCMM-26-2673-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/256b/9077308/ffaaca2292f5/JCMM-26-2673-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/256b/9077308/0def5d6d9f00/JCMM-26-2673-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/256b/9077308/a075ae89fae3/JCMM-26-2673-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/256b/9077308/daf1b078090c/JCMM-26-2673-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/256b/9077308/86d8273ebce4/JCMM-26-2673-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/256b/9077308/ddb38f5889eb/JCMM-26-2673-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/256b/9077308/c468dad0cae5/JCMM-26-2673-g005.jpg

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