Constitutive activation of STAT3 and cyclin D1 overexpression contribute to proliferation, migration and invasion in gastric cancer cells.

Signal transducer and activator of transcription-3 (STAT3) is closely associated with tumorigenesis and is activated in tumor cells of a variety of cancers. The raised expression of cyclin D1 (CCND1) by activated STAT3 has been verified in some cancers. However, the relationship between STAT3 and CCND1 has yet to be studied in gastric cancer (GC) cells. In the present study, we found that STAT3 was constitutively activated in several GC cells together with overexpressed CCND1. In addition, IL-6 treatment enhanced the expression level of p-STAT3 and CCND1, accelerating the cell cycle progress and transferring from G1 to S phase. The increased proliferation, migration and invasion were also demonstrated by the treatment of IL-6 in HGC-27 and BGC-823 cells. While AG490 treatment, a Janus Kinase (JAK) inhibitor, showed the opposite effect. Therefore, our research demonstrated the positive correlation between p-STAT3 and CCND1 in GC cells. The constitutive activation of STAT3 and CCND1 overexpression accounted for the proliferation, migration and invasion in GC cells.