Malignant neoplasm of prostate
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In the Chinese population, the -94 ins/del ATTG polymorphism in NF-κ B1 promoter may contribute to the etiology of bladder cancer instead of renal cell carcinoma or prostate cancer.
|
26484607 |
2016 |
Malignant neoplasm of prostate
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In conclusion, polymorphisms in NFKB1 and NFKBIA genes may modulate the risk of developing prostate cancer among Chinese.
|
26068031 |
2015 |
Malignant neoplasm of prostate
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
ERβ regulation of NF-kB activation in prostate cancer is mediated by HIF-1.
|
26450901 |
2015 |
Malignant neoplasm of prostate
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
We showed that T/E fusion can activate NF-kB pathway by increasing phosphorylation of NF-kB p65 Ser536 (p536), but the function of p536 has never been studied in PCa.
|
25749044 |
2015 |
Malignant neoplasm of prostate
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In conclusion, NFKB1 -94 ins/del and COX-2 (-1195G>A) polymorphisms may be, respectively, associated with decreased and increased prostate cancer risk in the Chinese population.
|
26788504 |
2015 |
Malignant neoplasm of prostate
|
0.100 |
Biomarker
|
disease |
BEFREE |
Prostate cancer-derived BMP-6 stimulates tumor-associated macrophages to produce IL-1a through a crosstalk between Smad1 and NF-kB1; IL-1a, in turn, promotes angiogenesis and prostate cancer growth.
|
24185914 |
2014 |
Malignant neoplasm of prostate
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
A lowered risk for PC was also found for carriers of variant allele NFKB1 -94ins/delATTG among non-users of NSAIDs (IRR 0.68; 95% CI 0.47-0.99), for non-aggressive disease (IRR 0.64; 95% CI 0.42-0.99), and among men with a body mass index above 30 kg/m(2) (IRR 0.56; 95% CI 0.27-1.16), although the latter estimate was based on small numbers.
|
23880210 |
2013 |
Malignant neoplasm of prostate
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Among these genes, it appears that: PPARG promotes the PPAR signaling pathway via the upregulation of lipoprotein lipase (LPL) expression, but suppresses the cell cycle pathway via downregulation of growth arrest and DNA-damage-inducible, γ (GADD45G) expression; ETV4 stimulates matrix metallopeptidase 9 (MMP9) expression to induce the bladder cancer pathway; FLI upregulates transforming growth factor, β receptor II (TGFBR2) expression to activate TGF-β signaling and upregulates cyclin D3 (CCND3) expression to promote the cell cycle pathway; NFKB1 upregulates interleukin 1, β (IL-1B) expression and initiates the prostate cancer pathway; CEBPB upregulates IL-6 expression and promotes pathways in cancer; and TAL1 promotes kinase insert domain receptor (KDR) expression to promote the TGF-β signaling pathway.
|
22895549 |
2012 |
Malignant neoplasm of prostate
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The functional NFKB1 promoter polymorphism is associated with increased risk of prostate cancer.
|
19446741 |
2009 |
Malignant neoplasm of prostate
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The limited number of samples analyzed in those studies and the relative lack of NF-kappaB target genes identified in RNA expression microarray analyses of prostate cancer cells suggest that further studies will be required in order to determine if NF-kappaB actually plays a role in human prostate cancer development, and/or progression, and to characterize its potential as a therapeutic target.
|
14689584 |
2004 |
Malignant neoplasm of prostate
|
0.100 |
Biomarker
|
disease |
BEFREE |
We demonstrate by DNA microarray, RT-PCR, Western blot and immunofluorescence analyses that treatment of androgen-sensitive prostate cancer cells (LNCaP) with 10(-5) M RE for 48 hr downregulates prostate-specific antigen (PSA), AR co-activator ARA 24 and NF-kB p65.
|
12569576 |
2003 |
Malignant neoplasm of prostate
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Our data demonstrate for the first time that a combined aberrant activation of NF-kappaB p50 and p65 and AP-1 JunD and Fra-1 in androgen-independent prostate cancer cells results in deregulated IL-6 expression, suggesting a novel potential entry point for therapeutic intervention in prostate cancer.
|
12727841 |
2003 |