title: Classical and alternative nuclear factor-κB pathways: a comparison among normal prostate, benign prostate hyperplasia and prostate cancer.
abstract: Nuclear factor-κB (NF-κB) is controlled by the classical and alternative NF-κB pathways, the role of which in prostate cancer (PCa) is not clearly defined. To provide this missing translational link, we compared the classical and alternative NF-κB pathways in normal prostate, benign prostate hyperplasia (BPH) and PCa. Prostate specimens were divided into three groups: group A, PCa (n = 68); group B, BPH (n = 60); and group C, normal prostates (n = 15). The gene expression levels of NF-κB1 and NF-κB2 were determined by real-time quantitative RT-PCR. Additionally, we analyzed the expression and sub-cellular localization of phosphorylated P50 (p-P50) and phosphorylated P52 (p-P52) proteins by immunohistochemical staining. Furthermore, associations were made between NF-κB pathway proteins and patients' prognosis. Compared with BPH and normal prostate tissues, the expression of NF-κB1 gene was differentially down-regulated by >1.5-fold, whereas NF-κB2 gene was differentially up-regulated by >2-fold in PCa tissues. The proportion of p-P50 positive patients in group A (26.5%) was significantly lower than in group B (88.3%, p = 0.005) and C (100%, p = 0.002). The proportion of p-P52 positive patients in group A (42.6%) was significantly higher than in group B (11.7%, p = 0.009) and C (6.7%, p = 0.008). Comparison of the survival curves in group A according to p-P52 expression showed a significant difference between positive and negative patients. The p-P52 positive patients showed worse prognosis (p = 0.019). Our findings suggest for the first time that the classical and alternative NF-κB pathways have an important role in PCa. p-P52 might be a predictor of poor prognosis for PCa.
authors.affiliation: Department of Urology, Guangzhou First Municipal People's Hospital, Affiliated Guangzhou Medical College, Guangzhou 510180, China.
authors.forename: Chao
authors.initials: C
authors.lastname: Cai
authors.forename: Fu-neng
authors.initials: FN
authors.lastname: Jiang
authors.forename: Yu-xiang
authors.initials: YX
authors.lastname: Liang
authors.forename: Hui-chan
authors.initials: HC
authors.lastname: He
authors.forename: Zhao-dong
authors.initials: ZD
authors.lastname: Han
authors.forename: Qi-shan
authors.initials: QS
authors.lastname: Dai
authors.forename: Guo-qiang
authors.initials: GQ
authors.lastname: Qin
authors.forename: Jia-hong
authors.initials: JH
authors.lastname: Chen
authors.forename: Xi-bin
authors.initials: XB
authors.lastname: Chen
authors.forename: Yan-ru
authors.initials: YR
authors.lastname: Chen
authors.forename: Guo-hua
authors.initials: GH
authors.lastname: Zeng
authors.forename: Jian-guo
authors.initials: JG
authors.lastname: Zhu
authors.forename: Wei-de
authors.initials: WD
authors.lastname: Zhong
mesh_terms: D016022:Case-Control Studies; D015536:Down-Regulation; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D052002:NF-kappa B p50 Subunit / Q000235:genetics / Q000378:metabolism*; D052003:NF-kappa B p52 Subunit / Q000235:genetics / Q000378:metabolism*; D011379:Prognosis; D011467:Prostate / Q000378:metabolism*; D011470:Prostatic Hyperplasia / Q000235:genetics / Q000378:metabolism*; D011471:Prostatic Neoplasms / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction; D015854:Up-Regulation
chemical_list: D052002:NF-kappa B p50 Subunit; D052003:NF-kappa B p52 Subunit