Pancreatic cancer is one of the most fatal human cancers. Persistent and aberrant activation of signal transducer and activator of transcription 3 (STAT3) is the feature of many malignancies including the pancreatic cancer. Several studies reported that activated Stat3 maintains constitutive NF-kappaB activity. To determine mechanism of proliferation of pancreatic cancer cells, cell viability was examined using MTT assay. Expressions of total STAT3, phosphorylated STAT3, IkappaBalpha, cyclin D1 and survivin were determined by real-time PCR or Western blot analyses. NF-kappaB promoter activity was examined by luciferase assay. We found that activation of NF-kappaB and STAT3 as well as expression of STAT3-target genes cyclin D.sub.1 and survivin were induced in PANC-1 cells. These results indicate activation of STAT3 signaling pathway contributes to proliferation of pancreatic cancer cells. Therefore, targeting STAT3 may be beneficial for treating human pancreatic cancer.