Autor: |
Wang Q; OHIO STATE UNIV,DIV ENVIRONM HLTH SCI,SCH PUBL HLTH,COLUMBUS,OH 43210. OHIO STATE UNIV,DEPT PATHOL,COLUMBUS,OH 43210., Sabourin C, Kresty L, Stoner G |
Jazyk: |
angličtina |
Zdroj: |
International journal of oncology [Int J Oncol] 1996 Sep; Vol. 9 (3), pp. 473-9. |
DOI: |
10.3892/ijo.9.3.473 |
Abstrakt: |
Alterations in the expression of transforming growth factor-beta 1 (TGF-beta 1) have been implicated for malignancies of both human and experimental animal models. To further investigate the role of TGF-beta 1 in chemically-induced esophageal tumorigenesis, the expression of TGF-beta 1 was analyzed by reverse transcription-polymerase chain reaction (T-PCR) and immunohistochemical studies in N-nitrosomethylbenzylamine (NMBA)-induced rat esophageal tumorigenesis. We observed no significant difference in TGF-beta 1 mRNA levels between 25-week papillomas and normal rat esophageal epithelium. However, TGF-beta 1 mRNA levels were increased 2.9-fold (p<0.05) in 45-week papillomas induced by NMBA, when compared to normal rat esophageal epithelium. Immunohistochemical studies revealed a decreased intracellular TGF-beta 1 immunoreactivity in the papillomas when compared to the normal rat esophageal epithelium, indicating the existence of a discordance between TGF-beta 1 mRNA and protein expression. Furthermore, by immunohistochemical staining of proliferating cell nuclear antigen (PCNA), a predominantely mutually exclusive staining pattern was observed for TGF-beta 1 and PCNA. These findings suggest that overexpression of TGF-beta 1 mRNA occurs late in NMBA-induced rat esophageal tumorigenesis, and the discordant mRNA and protein expression may result in tumor evasion from TGF-beta 1 controlled negative growth regulation, thus promoting tumor progression in this model. |
Databáze: |
MEDLINE |
Externí odkaz: |
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