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Literature summary for 1.14.11.16 extracted from

  • Barboro, P.; Benelli, R.; Tosetti, F.; Costa, D.; Capaia, M.; Astigiano, S.; Vene, R.; Poggi, A.; Ferrari, N.
    Aspartate beta-hydroxylase targeting in castration-resistant prostate cancer modulates the NOTCH/HIF1alpha/GSK3beta crosstalk (2020), Carcinogenesis, 41, 1246-1252 .
    View publication on PubMed
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Application

Application Comment Organism
medicine ASPH gene alterations have prognostic value both in prostate cancer and castration-resistant prostate cancer patients. ASPH expression promotes a more aggressive malignant phenotype. In castration-resistant prostate cancer cells, inhibition of ASPH expression reduces cell proliferation, invasion and cyclin D1 expression through modulation of the NOTCH signaling. ASPH and HIF1alpha crosstalk might be transiently driven by the oxidative stress evidenced inside castration-resistant prostate cancer cells. ASPH silencing leads to increased phosphorylation of GSK3beta Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
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Source Tissue

Source Tissue Comment Organism Textmining
DU-145 cell
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 Homo sapiens
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LNCaP cell
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 Homo sapiens
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PC-3 cell
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 Homo sapiens
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