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BP‑1‑102, a novel inhibitor of signal transducer and activator of transcription 3 (STAT3), exhibits significant antitumor effects in several malignancies in vitro and in vivo. However, its role in gastric cancer (GC) remains to be elucidated. In the present study, the effect and potential molecular mechanisms of BP‑102 in human GC cell lines were investigated. The results showed that BP‑1‑02 dose‑dependently inhibited the proliferation of AGS cells, whereas it had little effect on HGC‑27 cells. Flow cytometric analysis indicated that BP‑1‑102 induced apoptosis, but had minimal effect on cell cycle distribution. In addition, cells treated with BP‑1‑102 demonstrated markedly suppressed migration and invasion capacities. Western blot analysis revealed that BP‑1‑102 inhibited the phosphorylation of STAT3 and its target genes, including c‑Myc, cyclin D1 and survivin, in a time‑ and dose‑dependent manner. Furthermore, it was found that BP‑1‑102 induced the phosphorylation of c‑Jun N‑terminal kinase and p38 mitogen‑activated protein kinase (MAPK) and inhibited the activation of extracellular signal‑related kinases. Taken together, these results demonstrated that BP‑1‑102 may be a potent antitumor agent that acts through modulating the STAT3 and MAPK signaling pathways in GC cells.

BP‑1‑102 exerts an antitumor effect on the AGS human gastric cancer cell line through modulating the STAT3 and MAPK signaling pathways