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TMSB10通过免疫微环境调节驱动前列腺癌的侵袭性。

TMSB10 drives prostate cancer aggressiveness via immune microenvironment regulation.

作者信息

Xia Haoran, Ning Jiaxin, Guo Xiaoxiao, Song Hongchen, Li Xuanhao, Wang Xuan

机构信息

Department of Urology, Beijing Friendship hospital, Capital Medical University, Beijing, P. R. China.

Institute of Urology, Beijing Municipal Health Commission, Beijing, P. R. China.

出版信息

Mol Med. 2025 Apr 30;31(1):160. doi: 10.1186/s10020-025-01211-8.

DOI:10.1186/s10020-025-01211-8
PMID:40307738
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12042486/
Abstract

Thymosin β10 (TMSB10) has emerged as a key player in the progression of prostate cancer, significantly influencing the tumor immune microenvironment. Pan-cancer analysis from The Cancer Genome Atlas (TCGA) revealed that TMSB10 is upregulated across multiple cancer types, particularly in prostate cancer, where high TMSB10 expression correlates with poorer patient outcomes. Functional assays using prostate cancer cell lines LNCaP and DU145 showed that TMSB10 silencing suppresses cell proliferation, migration, and invasion, while overexpression enhances these oncogenic processes. Furthermore, co-culture experiments demonstrated that TMSB10 overexpression skews macrophage polarization, decreasing the population of M1-type macrophages while increasing M2-type macrophages. This shift reduces immune cell cytotoxicity and alters cytokine secretion, highlighting TMSB10's role in immune evasion. These findings establish TMSB10 as a pivotal factor in prostate cancer biology, promoting tumor aggressiveness and modulating the immune response within the tumor microenvironment. TMSB10 presents a promising therapeutic target for prostate cancer, offering new avenues for treatments aimed at altering the tumor immune landscape. This research also provides a foundation for further exploration of TMSB10's role in other cancers.

摘要

胸腺素β10（TMSB10）已成为前列腺癌进展中的关键因素，对肿瘤免疫微环境有显著影响。癌症基因组图谱（TCGA）的泛癌分析显示，TMSB10在多种癌症类型中均上调，尤其是在前列腺癌中，TMSB10高表达与患者较差的预后相关。使用前列腺癌细胞系LNCaP和DU145进行的功能试验表明，TMSB10沉默可抑制细胞增殖、迁移和侵袭，而过表达则增强这些致癌过程。此外，共培养实验表明，TMSB10过表达会使巨噬细胞极化发生偏移，减少M1型巨噬细胞的数量，同时增加M2型巨噬细胞的数量。这种转变降低了免疫细胞的细胞毒性并改变了细胞因子分泌，突出了TMSB10在免疫逃逸中的作用。这些发现确立了TMSB10作为前列腺癌生物学中的关键因素，促进肿瘤侵袭性并调节肿瘤微环境中的免疫反应。TMSB10是前列腺癌一个有前景的治疗靶点，为旨在改变肿瘤免疫格局的治疗提供了新途径。这项研究还为进一步探索TMSB10在其他癌症中的作用奠定了基础。

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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38a6/12042486/a9704c655625/10020_2025_1211_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38a6/12042486/751086c72422/10020_2025_1211_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38a6/12042486/8b06c996f6f9/10020_2025_1211_Fig8_HTML.jpg
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本文引用的文献

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Castration-Resistant Prostate Cancer: From Uncovered Resistance Mechanisms to Current Treatments.去势抵抗性前列腺癌：从未被揭示的抵抗机制到当前的治疗方法
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Pan-cancer analysis identifies the correlations of Thymosin Beta 10 with predicting prognosis and immunotherapy response.泛癌症分析确定了胸腺素β 10 与预测预后和免疫治疗反应的相关性。
Front Immunol. 2023 May 18;14:1170539. doi: 10.3389/fimmu.2023.1170539. eCollection 2023.
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Thymosin Beta 4 Inhibits LPS and ATP-Induced Hepatic Stellate Cells via the Regulation of Multiple Signaling Pathways.胸腺素β4 通过调节多条信号通路抑制 LPS 和 ATP 诱导的肝星状细胞。
Int J Mol Sci. 2023 Feb 8;24(4):3439. doi: 10.3390/ijms24043439.
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Integration of scRNA-Seq and Bulk RNA-Seq Reveals Molecular Characterization of the Immune Microenvironment in Acute Pancreatitis.单细胞 RNA 测序和批量 RNA 测序的整合揭示了急性胰腺炎免疫微环境的分子特征。
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Docetaxel versus abiraterone for metastatic hormone-sensitive prostate cancer with focus on efficacy of sequential therapy.多西他赛与阿比特龙治疗转移性激素敏感前列腺癌的疗效比较：序贯治疗的作用。
Prostate. 2023 May;83(6):563-571. doi: 10.1002/pros.24488. Epub 2023 Jan 20.
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Management of patients with advanced prostate cancer in Japan: 'real-world' consideration of the results from the Advanced Prostate Cancer Consensus Conference.日本晚期前列腺癌患者的管理：对晚期前列腺癌共识会议结果的“真实世界”考量
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