Studies have shown that stromal interaction molecule 1 (STIM1) is expressed in a variety of cancers and is related to tumor growth. The present study aimed to investigate the expression and roles of STIM1 in gastric carcinoma. Immunohistochemistry and western blotting revealed that STIM1 was expressed at higher levels in gastric cancer tissues (82%) than these levels in normal gastric tissues (42%). In addition, STIM1 was also expressed in tumor vascular endothelial cells. The effects of STIM1 on proliferation, apoptosis, adhesion, invasion and migration of gastric cancer cells were detected by MTT assay, flow cytometry, cell adhesion assay and Transwell assay, respectively. The results shown that STIM1 knockdown did not alter proliferation or apoptosis, but promoted cell adhesion and inhibited migration and invasion in the gastric cancer cells. In addition, STIM1 knockdown did not alter the expression or phosphorylation of mitogen-activated protein kinase (MEK) or extracellular signal-regulated kinase (ERK), implying that STIM1 affected gastric cancer cell migration through a pathway independent of the MEK/ERK pathway.