Tumor-derived exosomes (TDEs) have been shown to impede anti-tumor immune responses via their immunosuppressive cargo. Since dendritic cells (DCs) are the key mediators of priming and maintenance of T cell-mediated responses; thus it is logical that the exosomes released by tumor cells can exert a dominant influence on DCs biology. This paper intends to provide a mechanistic insight into the TDEs-mediated DCs abnormalities in the tumor context. More importantly, we discuss extensively how tumor exosomes induce subversion of DCs differentiation, maturation and function in separate sections. We also briefly describe the importance of TDEs at therapeutic level to help guide future treatment options, in particular DC-based vaccination strategy, and review advances in the design and discovery of exosome inhibitors. Understanding the exosomal content and the pathways by which TDEs are responsible for immune evasion may help to revise treatment rationales and devise novel therapeutic approaches to overcome the hurdles in cancer treatment.
Tumor-derived exosomes (TDEs) play pivotal roles in several aspects of cancer biology. It is now evident that TDEs also favor tumor growth by negatively affecting anti-tumor immunity. As important sentinels of immune surveillance system, natural killer (NK) cells can recognize malignant cells very early and counteract the tumor development and metastasis without a need for additional activation. Based on this rationale, adoptive transfer of ex vivo expanded NK cells/NK cell lines, such as NK-92 cells, has attracted great attention and is widely studied as a promising immunotherapy for cancer treatment. However, by exploiting various strategies, including secretion of exosomes, cancer cells are able to subvert NK cell responses. This paper reviews the roles of TDEs in cancer-induced NK cells impairments with mechanistic insights. The clinical significance and potential approaches to nullify the effects of TDEs on NK cells in cancer immunotherapy are also discussed.
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MiRNAs that are characterized by small non-coding RNAs orchestrate the expression of important genes involved in cancer cell development processes including apoptosis, proliferation, angiogenesis, metastasis, and drug resistance at the post-transcriptional level. Dysregulation of miR-9 in various cancers has been reported. Recently, miR-9 has been considered as a key miRNA in various malignancies. However its importance in the pathogenesis of different neoplasms is not yet well defined. Accordingly, this study was conducted in order to clarify the potential roles of miR-9 in in the development of various cancers, prognosis, and treatment approaches. We have shown that a large number of miR-9 targets play fundamental roles in carcinogenesis and that is dysregulated in various cancer cells. Our findings was found aberrant miR-9 expression in a majority of cancers. This review article, generally emphasize on the critical roles of miR-9 in cancer cell progression. Additionally, we intended to investigate the effects of down-regulation or up-regulation of miR-9 in different types of cancers. It is hoped that a good understanding of the regulatory roles of miR-9 in various cancers be helpful for using miR-9 in the clinical settings including prognosis, diagnose, and miRNA based target therapy.
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