2-Chloromethyl anthraquinone inhibits Candida albicans biofilm formation by inhibiting the Ras1-cAMP-Efg1 pathway.

Candida albicans is an opportunistic pathogen, and the formation of its biofilm makes it resistant to traditional antifungal therapy. Anthraquinones have universal antibacterial activity. We evaluated the inhibitory effects of 2-chloromethyl anthraquinone on C. albicans adhesion, mycelial morphology transformation, and biofilm formation. The results showed that 2-chloromethyl anthraquinone could inhibit C. albicans adhesion, mycelium formation, and biofilm formation in a dose-dependent manner at 2 μg/mL. In addition, 2-chloromethyl anthraquinone significantly inhibited the expression of biofilm formation-related genes in C. albicans, including ALS1, CPH1, ECE1, HWP1, TEC1, BCR1, and UME6. In addition, Ras1-cAMP-Efg1 pathway-related genes (RAC1, CYR1, and TPK2) were also significantly down-regulated, indicating that the inhibitory effect of 2-chloromethyl anthraquinone on C. albicans biofilms may be related to the Ras1-cAMP-Efg1 signaling pathway. In summary, the results of this study confirmed the inhibitory mechanism of 2-chloromethyl anthraquinone on the virulence factors of C. albicans, which laid a theoretical foundation for its use as an anti-biofilm agent against C. albicans.