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Summary: Esophageal carcinoma (EC) is one of the most common malignant tumors in the world. ECRG4 has been recently discovered to be downregulated in EC. However, the mechanism leading to reduced expression of ECRG4 in esophageal cancer remains obscure. Here, we found that ECRG4 expression was significantly downregulated in EC tissues and cell lines. ECRG4 overexpression led to a significant decrease in proliferation in vitro and in vivo. Mechanistically, ECRG4 can activate IRF3/IFN-γ pathway. IFN-γ can promote the expression of miR-29b. MiR-29b reduces the expression of DNMT1. DNMT1 may affect the expression of ECRG4 by affecting the methylation of ECRG4 promoter. These results reveal ECRG4/IRF3/IFN-γ/miR-29b/DNMT1 positive feedback loop in esophageal carcinoma cells, which may become a potential therapeutic target for esophageal carcinoma.

Diabetes, a ruthless chronic metabolic disorder, is increasingly considered to jeopardize global well-being over the decades. Royal jelly (RJ) is a complex natural product secreted by worker bees containing a unique fatty acid known as 10-hydroxy-2-decenoic acid (10-HDA). This study aimed to verify the protective effect on cognitive function of RJ and 10-HDA in diabetic mice and explore the underlying mechanism. Briefly, our animal experiment results suggested that 10-HDA had a significant hypoglycemic effect and improved cognitive performance. Through western blotting, RJ and 10-HDA intervention notably increased Atg7, Atg16L1, Beclin-1, Atg5, Atg12, Atg3, and LC3-II expression and decreased p62 expression. Meanwhile, decreased mTOR expression and increased ULK1 expression were also observed in the 10-HDA intervention group. In conclusion, 10-HDA can regulate mTOR/ULK1 pathway to activate autophagy to alleviate hippocampal damage, thereby improving cognitive function in mice with diabetes, which may provide a new option for real-world cognitive impairment management.