Our study provides insights into the specific delivery of hAFSC-EVs into inflammatory macrophages and sheds light on the potential therapeutic applications of these EVs for regulating inflammatory macrophage phenotypes.
Notably, in vivo experiments illustrated the efficacy of baicalin-PMs in suppressing M1 macrophage polarization and restraining tumor growth in the context of Lenvatinib resistance in ATC. Overall, the comprehensive multi-omics analysis underlines the potential of baicalin-PMs in reversing Lenvatinib resistance by modulating M1 macrophage function and inhibiting the MET factor, thus offering a novel strategy and target for combatting ATC resistance to Lenvatinib.
4 months ago
Journal
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MET (MET proto-oncogene, receptor tyrosine kinase)
The underlying metabolic and molecular mechanisms revealed that MICA in tumor cells induced M2-like polarization through the PPAR/EHHADH pathway, which regulates the fatty acid oxidation (FAO) in macrophages. The metabolic gene EHHADH, which is associated with MICA, led to alterations in M2-like macrophages by promoting heightened fatty acid uptake and augmenting levels of FAO within macrophages.
MMRN1 is a critical BTSC-related biomarker that contributes to GBM progression by enhancing tumor stemness and modulating the immune microenvironment. Targeting MMRN1 May represent a promising therapeutic approach for GBM treatment.
Our findings revealed that PEITC significantly reduced MIF expression in GL-261 cells, both in culture and in orthotopic tumor tissue, and decreased MIF-induced cellular signaling. These results suggest that PEITC has potential to be a therapeutic agent for glioblastoma by inhibiting tumor growth and modulating the immune response through MIF suppression.