Sufentanil inhibits the metastasis and immune response of breast cancer via mediating the NF-κB pathway.

IF 2.9 4区医学 Q3 IMMUNOLOGY

Immunopharmacology and Immunotoxicology Pub Date : 2023-12-01 Epub Date: 2023-07-06 DOI:10.1080/08923973.2023.2228476

Mingming Li, Kuo Gu, Qingling Kong, Guonian Wang, Jing Gu

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引用次数: 0

Abstract

Objective: Breast cancer (BC) causes cancer-related death in women. Sufentanil is used for cancer pain and postoperative analgesia. This study aimed to explore the role of sufentanil in BC.

Methods: BC cells were treated with sufentanil, and cell viability was evaluated using the cell counting kit-8 (CCK-8) assay. Biological behaviors were analyzed using EDU assay, flow cytometry, transwell assay, western blotting, and ELISA. The levels of NF-κB pathway-related factors were examined using western blotting. A xenograft tumor model was established to assess the effects of sufentanil on tumor growth in vivo.

Results: Sufentanil at the concentration of 20, 40, 80, and 160 nM suppressed cell viability (IC50 = 39.84 in MDA-MB-231 cells, and IC50 = 47.46 in BT549 cells). Sufentanil inhibited the proliferation, invasion, epithelial-mesenchymal transition (EMT), and inflammation, but induced apoptosis of BC cells. Mechanically, sufentanil suppressed the activation of the NF-κB pathway. Rescue experiments showed that RANKL (NF-κB receptor agonist) abrogated the effects induced by sufentanil. Moreover, sufentanil inhibited tumor growth, inflammatory response, but promoted apoptosis via the NF-κB pathway in vivo.

Conclusions: Sufentanil decelerated the progression of BC by regulating the NF-κB pathway, suggesting sufentanil may be used in BC therapy.

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舒芬太尼通过介导NF-κB途径抑制癌症转移和免疫反应。

目的：癌症（BC）引起女性癌症相关死亡。舒芬太尼用于癌症疼痛和术后镇痛。本研究旨在探讨舒芬太尼在BC中的作用。方法：用舒芬太尼处理BC细胞，用细胞计数试剂盒-8（CCK-8）测定细胞活力。采用EDU法、流式细胞仪、transwell法、蛋白质印迹法和ELISA法对其生物学行为进行分析。采用蛋白质印迹法检测NF-κB通路相关因子的水平。建立了异种移植物肿瘤模型，以评估舒芬太尼对体内肿瘤生长的影响。结果：舒芬太尼浓度为20、40、80和160 nM抑制的细胞活力（IC50 = MDA-MB-231细胞中的39.84和IC50 = 在BT549细胞中为47.46）。舒芬太尼抑制BC细胞的增殖、侵袭、上皮-间质转化（EMT）和炎症，但诱导BC细胞凋亡。舒芬太尼在机制上抑制NF-κB通路的激活。拯救实验表明，RANKL（NF-κB受体激动剂）消除了舒芬太尼诱导的效应。此外，舒芬太尼在体内抑制肿瘤生长和炎症反应，但通过NF-κB途径促进细胞凋亡。结论：舒芬太尼通过调节NF-κB通路减缓BC的进展，提示舒芬太尼可用于BC的治疗。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Immunopharmacology and Immunotoxicology 医学-毒理学

CiteScore

5.40

自引率

0.00%

发文量

133

审稿时长

4-8 weeks

期刊介绍： The journal Immunopharmacology and Immunotoxicology is devoted to pre-clinical and clinical drug discovery and development targeting the immune system. Research related to the immunoregulatory effects of various compounds, including small-molecule drugs and biologics, on immunocompetent cells and immune responses, as well as the immunotoxicity exerted by xenobiotics and drugs. Only research that describe the mechanisms of specific compounds (not extracts) is of interest to the journal. The journal will prioritise preclinical and clinical studies on immunotherapy of disorders such as chronic inflammation, allergy, autoimmunity, cancer etc. The effects of small-drugs, vaccines and biologics against central immunological targets as well as cell-based therapy, including dendritic cell therapy, T cell adoptive transfer and stem cell therapy, are topics of particular interest. Publications pointing towards potential new drug targets within the immune system or novel technology for immunopharmacological drug development are also welcome. With an immunoscience focus on drug development, immunotherapy and toxicology, the journal will cover areas such as infection, allergy, inflammation, tumor immunology, degenerative disorders, immunodeficiencies, neurology, atherosclerosis and more. Immunopharmacology and Immunotoxicology will accept original manuscripts, brief communications, commentaries, mini-reviews, reviews, clinical trials and clinical cases, on the condition that the results reported are based on original, clinical, or basic research that has not been published elsewhere in any journal in any language (except in abstract form relating to paper communicated to scientific meetings and symposiums).