Key result
Testosterone and 17beta-estradiol reversed the inhibitory effects of angiotensin 1-7 and angiotensin II, respectively, on protein tyrosine kinase activity in DU145 prostate cancer cells.
Why the study?
Do testosterone and 17β-estradiol modify angiotensin-induced changes in protein tyrosine kinase activity in DU145 prostate cancer cells?
Do testosterone and 17β-estradiol modify angiotensin-induced changes in protein tyrosine kinase activity in DU145 prostate cancer cells?
p-value: p=<0.05
Testosterone and 17β-estradiol reverse the inhibitory action of angiotensins on protein tyrosine kinase activity in DU145 prostate cancer cells, suggesting a rapid non-genomic mechanism that may contribute to cancer progression.
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No immediate clinical implications in prostate cancer; leaves open non-genomic steroid-angiotensin effects on tumor kinase activity.
Domińska et al. (2017) studied Prostate cancer. Testosterone and 17beta-estradiol vs. Control (cyclodextrin alone) was evaluated on Protein tyrosine kinase (PTK) activity (p=<0.05). Testosterone and 17beta-estradiol reversed the inhibitory effects of angiotensin 1-7 and angiotensin II, respectively, on protein tyrosine kinase activity in DU145 prostate cancer cells.
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