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BAIAP2L2通过GABPB1介导的活性氧失衡促进肝细胞癌的恶性发展。

BAIAP2L2 promotes the malignancy of hepatocellular carcinoma via GABPB1-mediated reactive oxygen species imbalance.

作者信息

Jia Wenbo, Xu Bin, Yu Liang, Feng Yanzhi, Wang Jinyi, Xu Chao, Liang Litao, Zhou Yongping, Ding Wenzhou, Kong Lianbao

机构信息

Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.

Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, National Health Commission (NHC) Key Laboratory of Hepatobiliary Cancers, Nanjing, Jiangsu Province, China.

出版信息

Cancer Gene Ther. 2024 Dec;31(12):1868-1883. doi: 10.1038/s41417-024-00841-0. Epub 2024 Nov 4.

DOI:10.1038/s41417-024-00841-0
PMID:39496939
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11645275/
Abstract

Hepatocellular carcinoma (HCC) is a common type of cancer worldwide and ranks as the fourth leading cause of cancer-related deaths. This research investigation identified an upregulation of BAI1-associated protein 2-like 2 (BAIAP2L2) in HCC tissues, which was found to be an independent prognostic factor for overall survival in HCC patients. BAIAP2L2 was observed to enhance cell proliferation, metastasis, stemness, cell cycle progression, and inhibit apoptosis in HCC. Mechanistically, NFκB1 was found to stimulate BAIAP2L2 transcription by directly binding to its promoter region. BAIAP2L2 interacts with GABPB1 to inhibit its ubiquitin-mediated degradation and promote its nuclear translocation. BAIAP2L2 inhibits the levels of reactive oxygen species (ROS) by regulating GABPB1, thereby promoting cancer properties in HCC and reducing the sensitivity of HCC to lenvatinib. In summary, this study elucidates the role and underlying mechanism of BAIAP2L2 in HCC, providing a potential biomarker and therapeutic target for this disease.

摘要

肝细胞癌（HCC）是全球常见的癌症类型，也是癌症相关死亡的第四大主要原因。本研究调查发现，HCC组织中BAI1相关蛋白2样2（BAIAP2L2）上调，这被发现是HCC患者总生存期的独立预后因素。观察到BAIAP2L2可增强HCC中的细胞增殖、转移、干性、细胞周期进程并抑制细胞凋亡。机制上，发现NFκB1通过直接结合其启动子区域来刺激BAIAP2L2转录。BAIAP2L2与GABPB1相互作用，抑制其泛素介导的降解并促进其核转位。BAIAP2L2通过调节GABPB1来抑制活性氧（ROS）水平，从而促进HCC中的癌症特性并降低HCC对乐伐替尼的敏感性。总之，本研究阐明了BAIAP2L2在HCC中的作用及潜在机制，为该疾病提供了一个潜在的生物标志物和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5623/11645275/655bfd89cb19/41417_2024_841_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5623/11645275/2f73a19a49b2/41417_2024_841_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5623/11645275/f01dca97fb84/41417_2024_841_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5623/11645275/eb6fa3168484/41417_2024_841_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5623/11645275/73a829406e6e/41417_2024_841_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5623/11645275/8e9a85b2635b/41417_2024_841_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5623/11645275/cbaa2508cc9e/41417_2024_841_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5623/11645275/7460ecefe2a1/41417_2024_841_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5623/11645275/655bfd89cb19/41417_2024_841_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5623/11645275/2f73a19a49b2/41417_2024_841_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5623/11645275/f01dca97fb84/41417_2024_841_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5623/11645275/eb6fa3168484/41417_2024_841_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5623/11645275/73a829406e6e/41417_2024_841_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5623/11645275/8e9a85b2635b/41417_2024_841_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5623/11645275/cbaa2508cc9e/41417_2024_841_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5623/11645275/7460ecefe2a1/41417_2024_841_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5623/11645275/655bfd89cb19/41417_2024_841_Fig8_HTML.jpg

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本文引用的文献

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HOMER3 promotes non-small cell lung cancer growth and metastasis primarily through GABPB1-mediated mitochondrial metabolism. Homer3 通过 GABPB1 介导的线粒体代谢促进非小细胞肺癌生长和转移。
Cell Death Dis. 2023 Dec 11;14(12):814. doi: 10.1038/s41419-023-06335-5.
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BAIAP2L2 is a novel prognostic biomarker related to migration and invasion of HCC and associated with cuprotosis.BAIAP2L2 是一种与 HCC 迁移和侵袭相关的新型预后生物标志物，与铜死亡有关。
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Hypoxia-responsive PPARGC1A/BAMBI/ACSL5 axis promotes progression and resistance to lenvatinib in hepatocellular carcinoma.
缺氧反应性 PPARGC1A/BAMBI/ACSL5 轴促进肝癌的进展和对乐伐替尼的耐药性。
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Ferroptosis is induced by lenvatinib through fibroblast growth factor receptor-4 inhibition in hepatocellular carcinoma.仑伐替尼通过抑制成纤维细胞生长因子受体 4 诱导肝癌细胞发生铁死亡。
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BAIAP2L2 promotes the proliferation, migration and invasion of osteosarcoma associated with the Wnt/β-catenin pathway.BAIAP2L2通过Wnt/β-连环蛋白信号通路促进骨肉瘤的增殖、迁移和侵袭。
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