DNA Damage Promotes TMPRSS2-ERG Oncoprotein Destruction and Prostate Cancer Suppression via Signaling Converged by GSK3β and WEE1.

TMPRSS2-ERG gene fusion occurs in approximately 50% of cases of prostate cancer (PCa), and the fusion product is a key driver of prostate oncogenesis. However, how to leverage cellular signaling to ablate TMPRSS2-ERG oncoprotein for PCa treatment remains elusive. Here, we demonstrate that DNA damage induces proteasomal degradation of wild-type ERG and TMPRSS2-ERG oncoprotein through ERG threonine-187 and tyrosine-190 phosphorylation mediated by GSK3β and WEE1, respectively.

Combined effects of cigarette smoking, alcohol drinking and eNOS Glu298Asp polymorphism on blood pressure in Chinese male hypertensive subjects.

Introduction: Genetic factors and lifestyle exposures, as well as their combinations, play important roles in the development of hypertension. We examined whether cigarette smoking, alcohol drinking and the Glu298Asp polymorphism of the endothelial nitric oxide synthase (eNOS) gene generate combined effects on blood pressure (BP) in hypertensive subjects.

Methods: A total of 342 essential hypertensive subjects were recruited from Susong community in Anhui province, China, from July 2017 to January 2018, and the plasma biochemical parameters and the genotype on Glu298Asp polymorphism were determined.

A positive association between the human tissue kallikerin gene A2233C polymorphism and blood pressure response to benazepril.

Background: It is generally believed that essential hypertension is influenced by both genetic and environmental factors, as well as their interactions. Tissue kallikrein encoded by the tissue kallikrein gene (KLK1) is a key serine proteinase of kallikrein-kinin system, which is capable of generating potent vasactive peptides, kinins, by selective cleavage of the kininogen substrate. It was reported that the A2233 → C polymorphism in KLK1 gene is associated with essential hypertension.