Yfm (51) Mp4
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oAds oncolytic adenovirus, oMV oncolytic measles virus, oHSV herpes simplex virus, SCID severe combined immunodeficiency, hMSC human MSC, BM-MSC bone marrow-drived MSC, FM-MSC fetal membrane MSC, AD-MSC adipose tissue-derived MSC, HU-MSC human umbilical cord-derived MSC, HCC human hepatocellular carcinoma. ALL acute lymphoblastic leukemia, GBM glioblastoma multiforme, NSCLC non-small-cell lung carcinoma, PDA pancreatic ductal adenocarcinoma, CRAD conditional replication oncolytic adenoviruses
MSCs feature as OVs carriers and mechanisms of MSC-released OVs in cancer treatment. OVs are maintained by MSCs from immune system responses. MSCs migrate to the tumor site via chemotaxis. There are two major methods by which OVs destroy tumors are direct cell death and the activation of anti-tumor immunity. Tumor cells secret and release DAMPs such as HSPs, calreticulin, uric acid, and ATP and cytokines including, IFNs, TNF-α and IL-12, and PAMPs, such as nucleic acids, proteins, and viral capsid elements as a result of OVs infection and oncolysis. These compounds help counteract the immunosuppressive condition of the TME by promoting the migration and activation of MQs, NK cells, DCs, and tumor-specific cytotoxic T cells. Normal cells antiviral response also includes type I IFN which can play a significant part in anti-cancer responses by triggering immune cells inside the TME. DAMPs damage-associated molecular patterns, HSPs heat shock proteins, ATP adenosine triphosphate, IFNs interferons, TNF-α tumor necrosis factor-α, PAMPs pathogen-associated molecular patterns, MQs macrophages, NK cells natural killer cells, DCs dendritic cells, TME tumor microenvironment
All authors contributed to the conception and the main idea of the work. NGD, AIG, MEA, AOZ, MJA, RSZ, MAJ, SAJA, and JAR drafted the main text, figures, and tables. MD supervised the work and provided the comments and additional scientific information. YSA, NMM, YFM, and RAS also reviewed and revised the text. All authors read and approved the final version of the work to be published. 781b155fdc