STAT3 regulation the expression of VEGF-D in HGC-27 gastric cancer cell.

OBJECTIVE

To explore the potential mechanism of vascular endothelial growth factor D (VEGF-D) contribution to the lymphangiogenesis was regulated by the signal transducer and activator of transcription 3 (STAT3).

METHODS

We detected the expression in GC tissue, adjacent non-tumor tissue, GC cell lines (AGS, SUN-1, KATO-III, BGC-823, MGC-803, SGC-7901, and HGC-27), and GES-1 cell line. STAT3 siRNA transfection and genome microarray were applied to demonstrate whether the expression of VEGF-D was mediated by the STAT3 in GC.

RESULTS

We showed the STAT3, pSTAT3, and VEGF-D expression in GC tissue was significantly higher than those in adjacent non-tumor tissue, respectively. In addition, both STAT3 and VEGF-D mRNA expression was much higher in each GC cell line than those in GES-1 cell line. With STAT3 siRNA transfection, we demonstrated that VEGF-D expression level decreased significantly in HGC-27 cell by using the genome microarray representing STAT3 potential regulation the VEGF-D expression.

CONCLUSION

STAT3, a novel signal transducer inactivating in the GC cell, can contribute to the lymph node metastasis by promoting lymphangiogenesis via up-regulation expression of VEGF-D.