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. 2023 Jan 12;40(3):749–764. doi: 10.1007/s11095-022-03465-x

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — JNP released TCZ retains bioactivity. (a) ELISA data showing effects of JNP released TCZ on sIL-6R detection. Twenty-four hour treatment of U937 conditioned medium with stock TCZ at doses of 1 μg/mL (p < 0.01) and 10 μg/mL (p < 0.05) as well as 1 μg/mL (p < 0.05) released from JNP were associated with a significant decrease in sIL-6R secretion from U937 cells. (b) Similarly, TCZ treatment significantly reduced intracellular levels of IL-6R in treated U937 cells. (c) TCZ has shown numerous anti-tumorigenic effects through its modulation and inhibition of STAT3 via both classic (left pane) and trans-signaling (right pane). The JAK-STAT pathway favors tumor cell proliferation, angiogenesis in the tumor microenvironment, and metastasis (d) TCZ inhibits STAT3 phosphorylation by competitively binding to IL-6R (left pane) and sIl-6R (right pane) hence negating the downstream events. The target genes encode for proteins regulating growth and apoptosis. High concentrations of circulating IL-6 have been reported to increase resistance to both chemotherapy and radiation.