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AB180. The relationship between fructose-1, 6-bisphosphatase and hypoxia related genes expression in clear cell renal cell carcinoma
OBJECTIVE: Fructose-1,6-bisphosphatase (FBP1) is often known as a rate-limiting enzyme in gluconeogenesis. Recently, its catalytic activity-independent function, repress hypoxia induced factor (HIF) in the nucleus, was identified. The aim of this study was to investigate the relationship between FBP...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
AME Publishing Company
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4708732/ http://dx.doi.org/10.3978/j.issn.2223-4683.2015.s180 |
Sumario: | OBJECTIVE: Fructose-1,6-bisphosphatase (FBP1) is often known as a rate-limiting enzyme in gluconeogenesis. Recently, its catalytic activity-independent function, repress hypoxia induced factor (HIF) in the nucleus, was identified. The aim of this study was to investigate the relationship between FBP1 and hypoxia related genes expression in clear cell renal cell carcinoma (ccRCC). METHODS: The expression levels of FBP1, HIF-1α, HIF-2α, erythropoietin (Epo) and carbonic anhydrase IX (CA9) were assessed by immunochemical staining in archival ccRCC paraffin blocks from 123 patients using the tissue microarray technique. The expression level of FBP1 was then correlated with clinicopathological factors and the expression levels of HIF-1α, HIF-2α, Epo and CA9. RESULTS: Clinicopathological factors including age, gender, TNM stage and Fuhrman grade were indifferent between the patients with low FBP1 expression and those with strong FBP1 expression in ccRCC. FBP1 expression level was positively correlated with the expression levels of HIF-1α (P=0.005) and Epo (P=0.010), but without correlation with the expression level of HIF-2α (P=0.123) and CA9 (P=0.513) in ccRCC tissues. CONCLUSIONS: Our findings may be useful for recognizing the association between FBP1 and hypoxia related genes expression and understanding the mechanisms of ccRCC tumorigenesis. |
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