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The present study aimed to determine whether maslinic acid effectively inhibits the proliferation of MKN28 cells, and to investigate the mechanisms underlying its antitumor functions. MKN28 cell viability was evaluated using a Cell Counting Kit-8, cell proliferation was analyzed by a colony formation assay and flow cytometry was used to investigate the rate of apoptosis. Western blot analysis was performed in order to determine the differential expression levels of Janus kinase (JAK), signal transducer and activator of transcription 3 (STAT3) and apoptosis associated proteins B-cell lymphoma 2 (Bcl-2), Bcl-2 associated X protein (Bax) and Bcl-2 associated agonist of cell death (Bad). Interleukin-6 (IL-6) concentration was evaluated using ELISA. IL-6 and anti-IL-6 antibodies were used to investigate the role of IL-6 in MKN28 cells treated with maslinic acid proliferation, and the STAT3 phosphorylation rates. The results demonstrated that maslinic acid treatment significantly reduced cell proliferation, induced apoptosis and was accompanied by a significant decrease in Bcl-2, Bax and Bad expression levels. Maslinic acid treatment also resulted in the downregulation of phosphorylated-STAT3 and JAK2, and significantly inhibited the protein expression of IL-6. Maslinic acid is able to inhibit MKN28 cell proliferation and the phosphorylation of STAT3 by downregulating the expression of IL-6. These results suggest that maslinic acid suppresses the growth of MKN28 cells by inducing apoptosis via its inhibition of the IL-6/JAK/STAT3 signaling cascade. [ABSTRACT FROM AUTHOR]