Published online Apr 28, 2025. doi: 10.3748/wjg.v31.i16.104920
Revised: February 25, 2025
Accepted: April 7, 2025
Published online: April 28, 2025
Processing time: 111 Days and 1.6 Hours
Hesperetin, a flavonoid predominantly present in citrus fruits, exhibits significant intervention effects on both the initiation and progression of gastric cancer. However, the specific mechanisms underlying this effect remain unclear.
To investigate the interventional role of hesperetin on N-methyl-N’-nitro-N-nitrosoguanidine (MNNG)-induced exosomes in inducing gastric carcinogenesis.
Bioinformatics technology was used to identify the critical molecular components underlying hesperetin-mediated inhibition of MNNG induced gastric carcinogenesis through exosomal circular RNA. Biological experiments were conducted to validate these findings.
Exosomes derived from TGES-1 cells (TGES-1-EX) significantly enhanced the proliferation, migration, invasion, epithelial-mesenchymal transition (EMT), and stemness of GES-1 cells. The oncogenic potential of TGES-1-EX was significantly diminished following hesperetin pretreatment. TGES-1-EX with overexpressed or knocked down circ0008274 was extracted and GES-1 cells were treated in combination with hesperetin or alone. Our investigation revealed that hesperetin exerted significant inhibitory effects on MNNG-induced gastric carcinogenesis by exosomal circ0008274. Bioinformatics prediction identified microRNA (miR)-526b-5p as a potential miRNA binding to circ0008274. Functional experiments demonstrated that hesperetin may mediate its intervention in MNNG-induced gastric cancer initiation by targeting miR-526b-5p through exosomal circ0008274. TGES-1-EX circ0008274 promoted the proliferation, EMT, and cancer stem cell-like characteristics in GES-1 cells through miR-526b-5p-mediated regulatory mechanisms.
Hesperetin exerted an interventional effect on the gastric carcinogenesis process, particularly through the modulation of exosomal circ0008274 and its interaction with miR-526b-5p.
Core Tip: Hesperetin, a citrus flavonoid, shows potential in inhibiting gastric cancer initiation and progression, but via unclear mechanisms. This study explored its role in countering N-methyl-N’-nitro-N-nitrosoguanidine-induced gastric carcinogenesis mediated by exosomal circular RNA. Bioinformatics and biological experiments revealed that exosomes from TGES-1 cells enhanced GES-1 cell proliferation, migration, invasion, epithelial-mesenchymal transition (EMT), and stemness, but hesperetin pretreatment significantly reduced these effects. Hesperetin targeted exosomal circ0008274, which interacts with microRNA-526b-5p, to inhibit cancer-inducing properties. Overexpression or knockdown of circ0008274 confirmed its role in promoting GES-1 cell proliferation, EMT, and stemness via miR-526b-5p. Hesperetin intervenes in gastric carcinogenesis by modulating the exosomal circ0008274/miR-526b-5p axis.