Title : Down-regulated CFTR During Aging Contributes to Benign Prostatic Hyperplasia.

Pub. Date : 2015 Aug

PMID : 25546515






4 Functional Relationships(s)
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1 The present study investigated the possible involvement of the cystic fibrosis transmembrane conductance regulator (CFTR), which has been previously shown to negatively regulate nuclear factor-kappaB (NF-kappaB)/cyclooxygenase 2 (COX2)/prostaglandin E2 (PGE2) pathway, in the pathogenesis of BPH. Dinoprostone nuclear factor kappa B subunit 1 Homo sapiens
2 The present study investigated the possible involvement of the cystic fibrosis transmembrane conductance regulator (CFTR), which has been previously shown to negatively regulate nuclear factor-kappaB (NF-kappaB)/cyclooxygenase 2 (COX2)/prostaglandin E2 (PGE2) pathway, in the pathogenesis of BPH. Dinoprostone nuclear factor kappa B subunit 1 Homo sapiens
3 Furthermore, suppression of CFTR led to increased expression of COX2 and over-production of PGE2 in a normal human prostate epithelial cell line (PNT1A) with elevated NF-kappaB activity. Dinoprostone nuclear factor kappa B subunit 1 Homo sapiens
4 The present results suggest that CFTR may be involved in regulating PGE2 production through its negative regulation on NF-kappaB/COX2 pathway in prostate epithelial cells, which consequently stimulates cell growth of prostate stromal cells. Dinoprostone nuclear factor kappa B subunit 1 Homo sapiens