Metformin inhibits NF-κB p65/RelA-NLRP3 inflammasome-IL-1β axis, attenuates lipid droplet accumulation, and reprograms CD14/CD16 expression in monocytes exposed to colorectal tumor-conditioned medium
Abstract
BACKGROUND: Colorectal cancer (CRC) generates a complex tumor microenvironment (TME) known to profoundly alter the function and phenotype of immune cells, including monocytes. Key aspects of this environment can be mimicked by tumor-conditioned medium (TCM). Metformin has emerged as a promising candidate to counteract TCM-induced immune and inflammatory dysregulation. Therefore, this study aimed to evaluate the effects of metformin on NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome expression, monocyte subset distribution, and lipid droplet (LD) accumulation upon exposure to colorectal TCM.
METHODS: Assays were performed on primary human monocytes exposed to colorectal TCM in the presence or absence of metformin.
RESULTS: TCM significantly increased nitric oxide (NO, p 0.05).
CONCLUSIONS: Our findings highlight metformin's selective immunometabolic reprogramming capacity in monocytes exposed to colorectal tumor-derived signals, supporting its potential as a context-specific immunomodulator. This study lays the groundwork for future translational research on metformin as an adjunctive agent in inflammation-driven tumor settings.
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