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肿瘤抑制因子SALL2可对抗乳腺癌的化疗耐药性。

The tumor suppressor SALL2 opposes chemotherapeutic resistance in breast cancer.

作者信息

Li Qiji, Li Chenxin, Zhang Yuhao, Zheng Zihan, Wang Yun, Yang Yingqian, Zhu Qingqing, Wang Rui, Xu Wanhui, Zhu Chengming, Tian Qin, Wang Meng, Ye Liping

机构信息

The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, 518107, China.

School of Medicine, Sun Yat-Sen University, Shenzhen, 518107, China.

出版信息

Mol Cell Biochem. 2025 May;480(5):2971-2983. doi: 10.1007/s11010-024-05155-1. Epub 2024 Nov 22.

DOI:10.1007/s11010-024-05155-1
PMID:39572504
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12048432/
Abstract

Chemotherapy continues to be the primary treatment for certain types of breast cancer. However, despite an initial positive response to chemotherapeutic agents, the development of resistance is inevitable. The exact molecular mechanisms underlying this phenomenon remain unclear. In this research, a significant downregulation of SALL2 expression was observed in chemo-resistant breast cancer, which was attributed to promoter methylation. Decreased SALL2 expression correlated significantly with poorer relapse-free survival in chemotherapy-treated patients with breast cancer. Functionally, SALL2 silencing induced a stem cell-like phenotype in breast cancer cells, fostering resistance to cisplatin both in vitro and in vivo. This resistance was mediated, at least in part, through the transcriptional regulation of BTG2, a negative regulator of stemness, achieved by direct binding to its promoter regions. These findings underscore the critical role of SALL2 in modulating cisplatin response and propose SALL2 as a potential prognostic biomarker for chemotherapy response in breast cancer.

摘要

化疗仍然是某些类型乳腺癌的主要治疗方法。然而，尽管对化疗药物最初有积极反应，但耐药性的出现是不可避免的。这种现象背后的确切分子机制仍不清楚。在本研究中，在化疗耐药的乳腺癌中观察到SALL2表达显著下调，这归因于启动子甲基化。SALL2表达降低与接受化疗的乳腺癌患者无复发生存期较差显著相关。在功能上，SALL2沉默在乳腺癌细胞中诱导出干细胞样表型，在体外和体内均增强了对顺铂的耐药性。这种耐药性至少部分是通过对干性负调节因子BTG2的转录调控介导的，该调控是通过直接结合其启动子区域实现的。这些发现强调了SALL2在调节顺铂反应中的关键作用，并提出SALL2作为乳腺癌化疗反应的潜在预后生物标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1d5/12048432/a04d8d9f4d7d/11010_2024_5155_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1d5/12048432/c6bf0c8e6467/11010_2024_5155_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1d5/12048432/20af4764bc54/11010_2024_5155_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1d5/12048432/c7224a6abdf6/11010_2024_5155_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1d5/12048432/25ae855b1a26/11010_2024_5155_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1d5/12048432/fc2c0fcccab2/11010_2024_5155_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1d5/12048432/a04d8d9f4d7d/11010_2024_5155_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1d5/12048432/c6bf0c8e6467/11010_2024_5155_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1d5/12048432/20af4764bc54/11010_2024_5155_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1d5/12048432/c7224a6abdf6/11010_2024_5155_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1d5/12048432/25ae855b1a26/11010_2024_5155_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1d5/12048432/fc2c0fcccab2/11010_2024_5155_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1d5/12048432/a04d8d9f4d7d/11010_2024_5155_Fig6_HTML.jpg

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本文引用的文献

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Casein kinase 2 phosphorylates and induces the SALL2 tumor suppressor degradation in colon cancer cells.
酪蛋白激酶 2 磷酸化并诱导结肠癌细胞中的 SALL2 肿瘤抑制因子降解。
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Deletion of Wild-type p53 Facilitates Bone Metastatic Function by Blocking the AIP4 Mediated Ligand-Induced Degradation of CXCR4.野生型p53的缺失通过阻断AIP4介导的配体诱导的CXCR4降解促进骨转移功能。
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