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使用佐剂芹菜素增强抗肿瘤免疫

英文原题:Boosting Anti-tumour Immunity Using Adjuvant Apigenin.

查看英文原题

Boosting Anti-tumour Immunity Using Adjuvant Apigenin.

PubMed 2023/01/01(内容时间) Anticancer Agents Med Chem Q3 · IF 2.6(JCR 2025)

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中文摘要

肿瘤内部的相互作用和分泌物在肿瘤生长和治疗中起着关键作用。免疫抑制细胞如调节性 T 细胞(Tregs)、髓源性抑制细胞(MDSCs)、肿瘤相关巨噬细胞(TAMs)和癌症相关成纤维细胞(CAFs)分泌某些物质,这些物质可导致抗肿瘤免疫的耗竭。为了激发抗肿瘤免疫,一方面需要抑制免疫抑制细胞的分泌和相互作用,另一方面需要刺激自然杀伤(NK)细胞和 CD8+ T 淋巴细胞的增殖和活化。芹菜素是一种具有抗癌特性的黄酮。新出现的证据表明,芹菜素不仅能调节癌细胞的死亡通路,还能刺激抗肿瘤免疫细胞释放死亡信号并抑制促肿瘤分子的释放。在这篇综述中,我们讨论了芹菜素与肿瘤微环境(TME)内各种细胞之间的相互作用。这些相互作用可能增强抗肿瘤免疫,从而提高免疫治疗等抗癌疗法的效率。

展开英文摘要原文

The interactions and secretions within the tumour have a pivotal role in tumour growth and therapy. Immunosuppressive cells such as regulatory T cells (Tregs), myeloid-derived suppressor cells (MDSCs), tumour-associated macrophages (TAMs), and cancer-associated fibroblasts (CAFs) secrete some substances, which can result in the exhaustion of anti-tumour immunity. To stimulate anti-tumour immunity, suppression of the secretion and interactions of immunosuppressive cells, on the other hand, stimulation of proliferation and activation of natural killer (NK) cells and CD8+ T lymphocytes are required.

Apigenin is a flavone with anticancer properties. Emerging evidence shows that not only does apigenin modulate cell death pathways in cancer cells but it also can stimulate anti-tumour immune cells to release death signals and suppress the release of tumour-promoting molecules. In this review, we discuss the interactions between apigenin and various cells within the tumour microenvironment (TME). These interactions may enhance anti-tumour immunity to improve the efficiency of anticancer remedies such as immunotherapy.

论文信息

作者
Huang J、Chen X、Chang Z、Xiao C、Najafi M
第一作者单位
College of Basic Medicine, Shaoyang University, Shaoyang 422000, China.China
通讯作者单位
Medical Technology Research Center, Institute of Health Technology, Kermanshah University of Medical Sciences, Kermanshah, Iran.Iran
文献类型
综述 · 非美国政府资助研究
期刊
Anti-cancer agents in medicinal chemistry2023
原文标识
PubMed 35616683 · DOI 10.2174/1871520622666220523151409