Marvelon抑制MC38肿瘤生长,促进抗肿瘤免疫

IF 3.2 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Fandi Kong , Yongyan Chen , Dantong Liu, Hongying Gao, Qiaoru Yi, Mengjuan Zhang, Dan Li
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引用次数: 0

摘要

结直肠癌是一种全球流行的致命恶性肿瘤,由于其异质性和治疗耐药性,对其提出了重要挑战。尽管口服避孕药已被证明可以降低结直肠癌的发病率,但其对CD8+ T细胞抗肿瘤作用的影响尚不清楚。本研究表明,避孕药物Marvelon在抗mc38肿瘤免疫中起重要作用。避孕药Marvelon在体内显著抑制MC38肿瘤生长。Marvelon治疗可促进CD8+肿瘤浸润淋巴细胞中IFN-γ的表达,但对其耗尽谱的影响不大。通过进一步研究Marvelon的主要成分炔雌醇和去氧孕酮的作用,我们发现炔雌醇可以增强1型细胞毒性T (Tc1)细胞中IFN-γ的产生,并显著抑制MC38肿瘤细胞的活力,而去氧孕酮的作用很小。这项研究不仅重新定义了口服避孕药的作用,而且为开发新的免疫治疗策略提供了有价值的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Marvelon suppresses MC38 tumor growth and promotes anti-tumor immunity
Colorectal cancer is a prevalent and deadly malignancy globally, posing an important challenge due to its heterogeneity and treatment resistance. Although oral contraceptives have been shown to reduce the incidence of colorectal cancer, their impact on the anti-tumor effect of CD8+ T cells remains unclear. Here we show that the contraceptive Marvelon plays an important role in anti-MC38 tumor immunity. The contraceptive Marvelon significantly inhibits MC38 tumor growth in vivo. Marvelon treatment promotes IFN-γ expression in CD8+ tumor infiltrating lymphocytes, but shows dispensable impact on their exhausted profile. By further investigating the effects of Marvelon’s primary components, Ethinylestradiol and Desogestrel, we reveal that Ethinylestradiol enhances IFN-γ production in Type 1 Cytotoxic T (Tc1) cells and significantly inhibits the viability of MC38 tumor cells, whereas Desogestrel exhibits minimal effects. This study not only redefines the role of oral contraceptives but also provides valuable insights for the development of novel immunotherapeutic strategies.
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来源期刊
Molecular immunology
Molecular immunology 医学-免疫学
CiteScore
6.90
自引率
2.80%
发文量
324
审稿时长
50 days
期刊介绍: Molecular Immunology publishes original articles, reviews and commentaries on all areas of immunology, with a particular focus on description of cellular, biochemical or genetic mechanisms underlying immunological phenomena. Studies on all model organisms, from invertebrates to humans, are suitable. Examples include, but are not restricted to: Infection, autoimmunity, transplantation, immunodeficiencies, inflammation and tumor immunology Mechanisms of induction, regulation and termination of innate and adaptive immunity Intercellular communication, cooperation and regulation Intracellular mechanisms of immunity (endocytosis, protein trafficking, pathogen recognition, antigen presentation, etc) Mechanisms of action of the cells and molecules of the immune system Structural analysis Development of the immune system Comparative immunology and evolution of the immune system "Omics" studies and bioinformatics Vaccines, biotechnology and therapeutic manipulation of the immune system (therapeutic antibodies, cytokines, cellular therapies, etc) Technical developments.
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