Background

This review focuses on exosomes derived from various cancer cells. The review discusses the possibility of differentiating macrophages in alternatively activated anti-inflammatory pro-tumorigenic M2 macrophage phenotypes and classically activated pro-inflammatory, anti-tumorigenic M1 macrophage phenotypes in the tumor microenvironment (TME). The review is divided into two main parts, as follows: (1) role of exosomes in alternatively activating M2-like macrophages-breast cancer-derived exosomes, hepatocellular carcinoma (HCC) cell-derived exosomes, lung cancer-derived exosomes, prostate cancer-derived exosomes, Oral squamous cell carcinoma (OSCC)—derived exosomes, epithelial ovarian cancer (EOC)—derived exosomes, Glioblastoma (GBM) cell-derived exosomes, and colorectal cancer-derived exosomes, (2) role of exosomes in classically activating M1-like macrophages, oral squamous cell carcinoma-derived exosomes, breast cancer-derived exosomes, Pancreatic-cancer derived modified exosomes, and colorectal cancer-derived exosomes, and (3) exosomes and antibody-dependent cellular cytotoxicity (ADCC). This review addresses the following subjects: (1) crosstalk between cancer-derived exosomes and recipient macrophages, (2) the role of cancer-derived exosome payload(s) in modulating macrophage fate of differentiation, and (3) intracellular signaling mechanisms in macrophages regarding the exosome’s payload(s) upon its uptake and regulation of the TME.

Evidence

Under the electron microscope, nanoscale exosomes appear as specialized membranous vesicles that emerge from the endocytic cellular compartments. Exosomes harbor proteins, growth factors, cytokines, lipids, miRNA, mRNA, and DNAs. Exosomes are released by many cell types, including reticulocytes, dendritic cells, B-lymphocytes, platelets, mast cells, and tumor cells. It is becoming clear that exosomes can impinge upon signal transduction pathways, serve as a mediator of signaling crosstalk, thereby regulating cell-to-cell wireless communications.

Conclusion

Based on the vesicular cargo, the molecular constituents, the exosomes have the potential to change the fate of macrophage phenotypes, either M1, classically activated macrophages, or M2, alternatively activated macrophages. In this review, we discuss and describe the ability of tumor-derived exosomes in the mechanism of macrophage activation and polarization.

中文翻译：

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肿瘤来源的外来体在巨噬细胞极化的调节中

背景

这篇综述着重于衍生自各种癌细胞的外泌体。这篇综述讨论了在肿瘤微环境（TME）中区分激活的抗炎促肿瘤原M2巨噬细胞表型和经典激活的促炎抗肿瘤M1巨噬细胞表型的可能性。综述分为以下两个主要部分：（1）外泌体在交替激活M2样巨噬细胞，乳腺癌衍生的外泌体，肝细胞癌（HCC）细胞衍生的外泌体，肺癌衍生的外泌体，前列腺癌中的作用来源的外泌体，口腔鳞状细胞癌（OSCC）来源的上皮细胞，卵巢上皮癌（EOC）来源的外泌体，胶质母细胞瘤（GBM）细胞来源的外泌体和结直肠癌的来源外泌体，（2）外泌体在经典激活M1样巨噬细胞，口腔鳞状细胞癌衍生的外泌体，乳腺癌衍生的外泌体，胰腺癌衍生的修饰外泌体和大肠癌衍生的外泌体中的作用，以及（3）外泌体和抗体-依赖性细胞毒性（ADCC）。这项审查解决以下主题：（1）癌症来源的外泌体与受体巨噬细胞之间的串扰，（2）癌症来源的外泌体有效载荷在调节巨噬细胞分化命运中的作用，以及（3）巨噬细胞的细胞内信号传导机制关于外泌体摄取和调节TME的有效载荷的信息。（3）外泌体和抗体依赖性细胞毒性（ADCC）。这篇综述针对以下主题：（1）癌症来源的外泌体与受体巨噬细胞之间的串扰，（2）癌症来源的外泌体有效载荷在调节巨噬细胞分化命运中的作用，以及（3）巨噬细胞的细胞内信号传导机制关于外泌体摄取和调节TME的有效载荷的信息。（3）外泌体和抗体依赖性细胞毒性（ADCC）。这篇综述针对以下主题：（1）癌症来源的外泌体与受体巨噬细胞之间的串扰，（2）癌症来源的外泌体有效载荷在调节巨噬细胞分化命运中的作用，以及（3）巨噬细胞的细胞内信号传导机制关于外泌体摄取和调节TME的有效载荷的信息。

证据

在电子显微镜下，纳米级囊泡表现为从胞吞细胞区室出来的专门的膜状囊泡。外泌体包含蛋白质，生长因子，细胞因子，脂质，miRNA，mRNA和DNA。外泌体由许多细胞类型释放，包括网状细胞，树突状细胞，B淋巴细胞，血小板，肥大细胞和肿瘤细胞。越来越明显的是，外泌体可以撞击信号转导途径，充当信号串扰的中介，从而调节细胞间的无线通信。

结论

基于囊泡的货物，分子成分，外泌体具有改变巨噬细胞表型命运的潜力，M1是经典活化的巨噬细胞，或者是M2，或者是活化的巨噬细胞。在这篇综述中，我们讨论并描述了巨噬细胞激活和极化机制中肿瘤来源的外来体的能力。