Mechanism of Troxerutin-Mediated Regulation of EGLN3/LRPPRC in B[a]P-Induced Lung Adenocarcinoma
EGLN3 was identified as a critical gene in B[a]P-induced LUAD, exhibiting significant overexpression in LUAD tissues and BEAS-2B-T cells, with an inverse correlation to patient survival. Silencing of EGLN3 markedly inhibited the proliferation, colony formation, migration, and invasion of LUAD and BEAS-2B-T cells. Overexpression of LRPPRC effectively reversed these inhibitory effects, indicating a functional interplay between EGLN3 and LRPPRC. Troxerutin was identified as a potential small-molecule compound targeting the EGLN3/LRPPRC axis, reducing their expression and interaction, and consequently suppressing the malignant behavior of LUAD and BEAS-2B-T cells.