<p>Stomach carcinoma represents a malignancy with high prevalence and poor prognosis. hsa_circ_0006156’s expression level, a specific circular RNA (circRNA), shows a significant reduction in gastric carcinoma tissues when contrasted with normal tissues. The variations in the expression of hsa_circ_0006156correlates with gastric cancer differentiation, lymph node metastasis, and patient prognosis, although the underlying mechanisms remain elusive. In our study, cells were engineered to overexpress hsa_circ_0006156, while nude mice bearing HGC-27 tumor xenografts were established. Cell viability was assessed via CCK-8 assays, RNA levels were quantified using qRT-PCR, migration capabilities utilized wound healing assays and transwell assays, ferroptosis levels were determined by assessing reactive oxygen species (ROS), Fe²⁺, malondialdehyde (MDA), and glutathione (GSH) levels. Furthermore, RNA binding levels were investigated using dual-luciferase reporter assays. Our experimental outcomes revealed that in gastric carcinoma cells where founded a diminished expression of hsa_circ_0006156, while upregulation of hsa_circ_0006156 discovered restrain the growth, mobility, and spread of stomach cancer cells. Additionally, overexpression of hsa_circ_0006156 induced ferroptosis and concurrently suppressed tumor growth in gastric cancer cells. Mediated by the interaction with hsa_circ_0006156 and NCOA4, miR-942-5p reduces ferroptosis activation in stomach cancer cells. In gastric cancer cells, our current findings suggest that via the hsa_circ_0006156/miR-942-5p/NCOA4 axis hsa_circ_0006156 induces ferroptosis.</p> Graphical Abstract <p></p>