Tian Yehong, Ma Yinjie, Li Xue, Lu Gang, Wang Shixin, Qiu Xiaowei, Du Xu
College of Acupuncture and Tuina, Shaanxi University of Chinese Medicine, Xianyang, China.
Oncology Department, Wangjing Hospital of China Academy of Chinese Medical Sciences, Beijing, China.
Front Oncol. 2025 May 22;15:1584722. doi: 10.3389/fonc.2025.1584722. eCollection 2025.
Triple-negative breast cancer (TNBC) is known for its aggressive nature and poor prognosis, primarily due to limited treatment options stemming from immune evasion mechanisms. This study aimed to explore the therapeutic potential of peritumoral electroacupuncture (EA) in inhibiting tumor growth in TNBC, particularly focusing on the immune mechanisms related to CD8+ T cell recruitment and the involvement of histone deacetylase 1 (HDAC1) within the tumor microenvironment (TME). By constructing TNBC model in mice, we observed that EA not only inhibited tumor growth but also increased the presence of intratumoral CD8+ T cells and CCL5. Additionally, the expression of HDAC1 was found to down-regulate by EA. Remarkably, when EA was combined with the romidepsin (a class I HDAC inhibitor), a synergistic effect observed, leading to a greater increase in intratumoral CD8+ T cells compared to either treatment alone, resulting in a tumor inhibition rate of 60.03%. Importantly, EA did not worsen systemic inflammation, as serum levels of pro-inflammatory cytokines remained stable throughout the intervention. These findings indicate that peritumoral EA can effectively enhance anti-tumor immunity within the TME by down-regulating HDAC1. This research highlights the potential of combining non-invasive therapies like EA with pharmacological agent as a promising strategy for improving outcomes in the management of TNBC, warranting further exploration of its clinical applications.
三阴性乳腺癌(TNBC)以其侵袭性和预后不良而闻名,这主要是由于免疫逃逸机制导致治疗选择有限。本研究旨在探讨瘤周电针(EA)在抑制TNBC肿瘤生长方面的治疗潜力,特别关注与CD8 + T细胞募集相关的免疫机制以及肿瘤微环境(TME)中组蛋白去乙酰化酶1(HDAC1)的作用。通过在小鼠中构建TNBC模型,我们观察到EA不仅抑制肿瘤生长,还增加了瘤内CD8 + T细胞和CCL5的数量。此外,发现EA可下调HDAC1的表达。值得注意的是,当EA与罗米地辛(一种I类HDAC抑制剂)联合使用时,观察到协同效应,与单独使用任何一种治疗相比,瘤内CD8 + T细胞增加得更多,肿瘤抑制率达到60.03%。重要的是,EA并未加重全身炎症,因为在整个干预过程中促炎细胞因子的血清水平保持稳定。这些发现表明,瘤周EA可通过下调HDAC1有效增强TME内的抗肿瘤免疫力。本研究强调了将EA等非侵入性疗法与药物制剂相结合作为改善TNBC治疗效果的有前景策略的潜力,值得进一步探索其临床应用。