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. 2023 Mar 3;21(6):614–627. doi: 10.1158/1541-7786.MCR-22-0370

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©2023 The Authors; Published by the American Association for Cancer Research

This open access article is distributed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) license.

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Figure 7. JMJD6 molds TME through ANXA1-dependent macrophages polarization. JMJD6 favors ANXA1 expression, intracellular accumulation, through a pathway involving PPARα and ERα, and its increase in the TME. ANXA1 released by cancer cells triggers the conversion of macrophages to a pro-tumor M2-like state which favors tumor development. — JMJD6 molds TME through ANXA1-dependent macrophages polarization. JMJD6 favors ANXA1 expression, intracellular accumulation, through a pathway involving PPARα and ERα, and its increase in the TME. ANXA1 released by cancer cells triggers the conversion of macrophages to a pro-tumor M2-like state which favors tumor development.