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. 2018 Sep 21;9:1857. doi: 10.3389/fimmu.2018.01857

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Copyright © 2018 Phinney, Ray, Peretti, Jerman, Grim, Pinchuk and Beswick.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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MCP-1, Mip-1α, and Mip-2α (MMM) activate MK2 signaling and downstream cytokine expression in colon cancer cells. CT26 cells treated with MMM induce (A) MK2 phosphorylation. MK2i treatment inhibits (B) IL-1β, (C) IL-6, and (D) TNF-α in tumor supernatants, but this effect is reversed upon addition of MMM when examined by multiplex cytokine array. (E) Additional mRNA data for IL-1β and TNF-α since the protein level is low support the increase in cytokine gene expression. (F) MK2 is also phosphorylated in CT26 tumors, is decreased at day 13 in tumors treated with MK2 inhibitor, and is restored by addition of MMM in tumor treated with MK2 inhibitors. N = 7–8 for tumors, * and **p ≤ 0.05.