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And these factors can contribute to tumor progression and the evasion of systemic immune surveillance (Albini and Sporn, 2007). In vitro and in vivo anti-tumor effects of Astragalus membranaceus. Currently, most anticancer drugs are based mainly on specific targeted or cytotoxic agents which were discovered by using the “one gene, one target, one disease” approach (Anighoro et al., 2014). The tumor microenvironment is a critical determinant of distant cancer metastasis (Mlecnik et al., 2016). Immune cells in the tumor microenvironment, including regulatory T cells, dendritic cells, MDSCs and TAMs, are known to express a low level of MHC class I molecules but high levels of various immunosuppressive factors, such as IL-10, IL-6, and TGF-β. doi: 10.1016/j.canlet.20 Pub Med Abstract | Cross Ref Full Text | Google Scholar Deep, G., and Agarwal, R. Targeting tumor microenvironment with silibinin: promise and potential for a translational cancer chemopreventive strategy. Phytochemicals or their derived compounds are being increasingly recognized as potentially potent complementary treatments for cancer. Among them, some phytochemicals are being actively evaluated for use as adjuvants in anticancer therapies. These findings suggest that phytochemicals or their derivatives confer a spectrum of different pharmacological activities, which contrasts with the current cytotoxic anticancer drugs commonly used in clinics. doi: 10.1016/20 Pub Med Abstract | Cross Ref Full Text | Google Scholar Furuta, S., Jeng, Y. In this review, we have collected together pertinent information from recent studies about the biochemical and cellular mechanisms through which specific phytochemicals regulate target immune systems in defined tumor microenvironments.
Some phytochemicals or herbal extracts have been shown to confer suppressive activity in controlling MDSC expansion.
For instance, shikonin and hypericin were found to induce immunogenic cell death of specific cancer cells, and this effect was able to further activate the recognition activity of tumor cells by the host immune system. IL-25 causes apoptosis of IL-25R-expressing breast cancer cells without toxicity to nonmalignant cells.