Background and Aims Studies have shown that miR-199b-3p is downregulated in gastric cancer tissues, while cysteine-rich transmembrane BMP regulator 1 (CRIM1) is upregulated in these tissues. However, the role and mechanism of miR-199b-3p in the biological behavior of gastric cancer cells are still unclear, as is its potential association with CRIM1. Therefore, this study was conducted to investigate whether there is an interaction between miR-199b-3p and CRIM1 and how they affect the function of gastric cancer cells.Methods qRT-PCR and immunohistochemistry were used to detect the expression levels of miR-199b-3p and CRIM1 in gastric cancer tissues and adjacent non-cancerous tissues. Gastric cancer MGC803 cells were used to assess changes in cell proliferation, invasion/migration abilities, and apoptosis rates after overexpression of miR-199b-3p (using miR-199b-3p mimics) or knockdown of CRIM1 (using si-CRIM1). Bioinformatics analysis was used to predict the targeting relationship between miR-199b-3p and CRIM1, which was further validated by dual-luciferase reporter assay and confirmed through Western blot analysis.Results The results of qRT-PCR indicated that, compared to adjacent non-cancerous tissues, miR-199b-3p expression was significantly lower in gastric cancer tissues, while CRIM1 expression was higher (both P<0.05). Immunohistochemistry results demonstrated positive expression of CRIM1 in cancerous tissues, while it was negative in non-cancerous tissues. Overexpression of miR-199b-3p or CRIM1 knockdown resulted in decreased proliferation and invasion/migration abilities of MGC803 cells, along with increased apoptosis rates (all P<0.05). Bioinformatics prediction and dual-luciferase reporter assays confirmed that CRIM1 is a target of miR-199b-3p. Western blot analysis showed that CRIM1 expression was significantly reduced after transfection with miR-199b-3p mimics (P<0.05).Conclusion CRIM1 is a target gene of miR-199b-3p, which can inhibit the proliferation, invasion, and migration of gastric cancer cells while promoting apoptosis by targeting and regulating CRIM1 activity. The miR-199b-3p/CRIM1 pathway may serve as a potential therapeutic target for gastric cancer.