The NPL4/DXO/cyclin D1 axis exert crucial role in BC cell growth and is associated with prognosis and may represent a potential therapeutic target for BC.
Amplification of CCND1 or alterations in c-myc/CCND1 early in bladder cancer may have clinical relevance in promoting and predicting progression to detrusor-muscle-invasive transitional cell carcinoma.
Further statistical analysis revealed significant associations between increased p21 levels and bladder cancer patients with no exposure to chemicals (p=0.048), as well as with patients with no artificial sweetener intake (p=0.012), and between increased Cyclin D1 levels and study subjects with no artificial sweetener intake (p=0.012).
Overall, the amplification frequency decreased with increasing genomic distance from CCND1, suggesting that, among the genes examined, CCND1 is the major target gene in the 11q13 amplicon in bladder cancer.
Suppression of PHLPP2 or FOXO1 by miR-135a, consisted with dysregulation of p21, p27, Cyclin D1 and Ki67, play important roles in bladder cancer progression.
Our data from bioinformatic and luciferase reporter gene assays identified that miR-5195-3p targeted the mRNA 3'-UTR of Krüppel-like factor 5 (KLF5), which is a proven proto-oncogene in bladder cancer. miR-5195-3p sharply reduced KLF5 expression and suppressed the expression or activation of its several downstream genes that are kinases improving cell survival or promoting cell cycle regulators, including ERK1/2, VEGFA, and cyclin D1.
Immunohistochemical expression of Ki-67, Cyclin D1, p16INK4a, and Survivin as a predictive tool for recurrence and progression-free survival in papillary urothelial bladder cancer pTa / pT1 G2 (WHO 1973).
Although CCND1 polymorphism is not able to serve as a prognostic marker for bladder cancer, the CCND1 variant A allele may recessively increase the risk of carcinoma in situ incidence in patients with superficial bladder cancer.
Tissue microarrays containing bladder cancer specimens (n=212) and adjacent normal bladder tissues (n=131) were immunostained using an antibody against cyclin D1.
Twenty-one paraffin-embedded bladder tumors were analyzed by conventional comparative genome hybridization and fluorescence in situ hybridization (FISH) with a cyclin D1 gene (CCND1)/centromere 11 dual-color probe.
The aim of this study was to establish the frequency of combinatorial and separate copy number changes of INK4A (9p21), erbB-1 (7p11), erbB-2 (17q17-21), CMYC (8q24), CCND1 (11q13) and ZNF217 (20q13) in urothelial tumors; a tissue microarray of 159 urothelial bladder tumors was analyzed by fluorescence in situ hybridization.
Although CCND1 polymorphism is not able to serve as a prognostic marker for bladder cancer, the CCND1 variant A allele may recessively increase the risk of carcinoma in situ incidence in patients with superficial bladder cancer.
Our meta-analysis provides evidence that the variant genotype of CCND1G870A showed a significant association in the occurrence of invasive bladder tumors in former and current smokers.
We conducted a population-based case-control study of incidence of bladder cancer among non-Hispanic whites in Los Angeles County to examine the relationship between CCND1 870A-->G genotypes and bladder cancer risk.
Different expression patterns of cyclin D1 and CDK2 indicate heterogeneity in the mechanisms of G1-->S transition deregulation in individual bladder tumors which may elicit differences in their biological and clinical behavior.
The knock-down of miR-576-3p significantly promoted the proliferation of bladder cancer cells by accelerating the progression of cell cycle and increased the expression of cyclin D1.
When stratifying for the race, our analysis suggested that CCND1G870A was associated with bladder cancer risk in Asians when using homogeneous codominant (OR = 1.72, 95% CI 1.34-2.20, P < 0.0001), recessive (OR = 1.46, 95% CI 1.21-1.77, P < 0.0001), dominant (OR = 1.36, 95% CI 1.10-1.69, P = 0.004), and allelic models (OR = 1.30, 95% CI 1.15-1.47, P < 0.0001) to analyze the data.