Group of Experimental Biotherapy and Diagnostic, Institute for Regenerative Medicine, Sechenov First Moscow State Medical University, 119991 Moscow, Russia.
World-Class Research Center "Digital Biodesign and Personalized Healthcare", Sechenov First Moscow State Medical University, 119991 Moscow, Russia.
Discov Med. 2023 Aug;35(177):458-475. doi: 10.24976/Discov.Med.202335177.47.
Glioblastoma multiforme is one of the most widespread and dangerous forms of brain tumor with high inflammation. The tumor microenvironment comprises diverse tumor cells, different types of immune cells, and the extracellular matrix. Inflammatory mediators like chemokines, cytokines, and growth factors possibly serve as a capable therapeutic target to quash their tumor-promoting properties in glioblastoma multiforme (GBM). Cytokines are a heterogeneous group of soluble functional proteins which are also associated with the induction and progression of tumors. These are supposed to have both pro-inflammatory (such as tumor necrosis factor-α (TNF-α), interleukin-17A (IL-17A), interferon-γ (IFN-γ), IL-4, IL-2, IL-6, IL-12, IL-13) and anti-inflammatory (such as transforming growth factor-β (TGF-β), IL-10, and granulocyte-macrophage colony-stimulating factor (GM-CSF)) actions and are the crucial communications channels in the tumor microenvironment. In the present minireview we discuss the tumor microenvironment and inflammatory mediators and focus on the involvement of cytokines in establishing communication with the tumor microenvironment. The presented data highlight the possible roles of cytokines in communication between glioblastoma cells and tumor microenvironment. Cytokines formed by immune cells protect the host organs while cytokines secreted by tumor cells are used for their advantage. Though the clinical trials with a number of immunotherapeutic agents are going on around the globe, there is still a requirement for thorough investigation of the regulatory mechanism managing GBM growth, recurrence, and tumor response to the therapy.
胶质母细胞瘤是最广泛和危险的脑肿瘤形式之一，具有高度炎症。肿瘤微环境包括多种肿瘤细胞、不同类型的免疫细胞和细胞外基质。趋化因子、细胞因子和生长因子等炎症介质可能成为一种有能力的治疗靶点，以抑制其在胶质母细胞瘤（GBM）中的促肿瘤特性。细胞因子是一组异质的可溶性功能蛋白，也与肿瘤的诱导和进展有关。这些细胞因子被认为具有促炎（如肿瘤坏死因子-α（TNF-α）、白细胞介素-17A（IL-17A）、干扰素-γ（IFN-γ）、IL-4、IL-2、IL-6、IL-12、IL-13）和抗炎（如转化生长因子-β（TGF-β）、IL-10 和粒细胞-巨噬细胞集落刺激因子（GM-CSF））作用，是肿瘤微环境中的重要通讯渠道。在本综述中，我们讨论了肿瘤微环境和炎症介质，并重点关注细胞因子在与肿瘤微环境建立通讯中的作用。所提出的数据强调了细胞因子在胶质母细胞瘤细胞与肿瘤微环境之间通讯中的可能作用。免疫细胞产生的细胞因子保护宿主器官，而肿瘤细胞分泌的细胞因子则被用于其自身的优势。尽管全球正在进行许多免疫治疗药物的临床试验，但仍需要深入研究管理 GBM 生长、复发和肿瘤对治疗反应的调节机制。
