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.
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.
Entities:
Keywords:
Stomach; lymphatic metastasis; neoplasm; signal transducer and activator of transcription 3; vascular endothelial growth factor
Authors: S J Mandriota; L Jussila; M Jeltsch; A Compagni; D Baetens; R Prevo; S Banerji; J Huarte; R Montesano; D G Jackson; L Orci; K Alitalo; G Christofori; M S Pepper Journal: EMBO J Date: 2001-02-15 Impact factor: 11.598
Authors: Philippe O Van Trappen; Dawn Steele; David G Lowe; Suhail Baithun; Nigel Beasley; Wilko Thiele; Herbert Weich; Jaya Krishnan; John H Shepherd; Michael S Pepper; David G Jackson; Jonathan P Sleeman; Ian J Jacobs Journal: J Pathol Date: 2003-12 Impact factor: 7.996