Signal transducers and activators of transcription 3 up-regulates vascular endothelial growth factor production and tumor angiogenesis in head and neck squamous cell carcinoma
| Autor: | Shizuo Komune, Muneyuki Masuda, Satoshi Toh, I. Bernard Weinstein, Yuichiro Kutratomi, Torahiko Nakashima, Ryuji Yasumatsu, Aya Ito, Hong Ying Ruan, Takahiro Wakasaki |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
STAT3 Transcription Factor
Vascular Endothelial Growth Factor A Cancer Research Angiogenesis Biology Neovascularization chemistry.chemical_compound Tumor Cells Cultured medicine Humans RNA Messenger RNA Neoplasm STAT3 Neoplasm Staging Neovascularization Pathologic Reverse Transcriptase Polymerase Chain Reaction medicine.disease Head and neck squamous-cell carcinoma Neoplasm Proteins Tongue Neoplasms Up-Regulation Gene Expression Regulation Neoplastic Vascular endothelial growth factor Vascular endothelial growth factor A Oncology chemistry Head and Neck Neoplasms Carcinoma Squamous Cell biology.protein Cancer research Oral Surgery medicine.symptom Vascular endothelial growth factor production |
| Zdroj: | Oral Oncology. 43:785-790 |
| ISSN: | 1368-8375 |
| DOI: | 10.1016/j.oraloncology.2006.10.007 |
| Popis: | Overexpression of vascular endothelial growth factor (VEGF) is associated with angiogenic phenotypes and poor prognosis of numerous tumors, including head and neck squamous cell carcinoma (HNSCC). However, the precise mechanism that causes VEGF overexpression in HNSCC remains unknown. Since there is evidence that a transcriptional factor, signal transducers and activators of transcription 3 (Stat3), is constitutively activated in HNSCC and this activation is significantly associated with aggressive phenotypes of this disease, we investigated the roles of Stat3 activation on VEGF production and tumor angiogenesis in HNSCC both in vitro and in clinical samples. VEGF promoter assays with YCU-H891 cells demonstrated that dominant negative Stat3 significantly inhibited VEGF promoter activity in the full length (-2279 to +54) and two truncated forms of VEGF promoter luciferase-reporter construct (-1179 to 54) or (-1014 to +54), which retain the putative Stat3 responsive elements (-849 to -842). However, this was not seen in the shorter construct (-794 to +54), which lacks the putative Stat3 responsive elements. In the derivative of YCU-891 cells that stably express dominant negative Stat3 protein, cellular levels of VEGF mRNA and VEGF protein were significantly inhibited. In the 51 clinical samples obtained from the patients with tongue carcinoma, the expression levels of phosphorylated (activated) form of Stat3 protein were significantly correlated with VEGF (P |
| Databáze: | OpenAIRE |
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