High expression of B23 is associated with tumorigenesis and poor prognosis in bladder urothelial carcinoma

Abstract

B23, a multifunctional nucleolar protein, is overexpressed in numerous cancers and is associated with tumorigenesis. However, the clinical significance and potential role of B23 in bladder urothelial carcinoma remains to be elucidated. The present study observed that the mRNA and protein expression levels of B23 were increased in bladder cancer cells and tissues. The overexpression of B23 contributed to tumorigenesis and was associated with poor prognosis in bladder cancer patients. Silencing of B23 by short hairpin RNA inhibited tumor cell growth and colony formation. In addition, knockdown of B23 suppressed the phosphorylation of extracellular signal-regulated kinase (ERK), resulting in the inactivation of the ERK signaling pathway. Therefore, the present study indicated that B23 promotes bladder cancer cell growth via activation of the ERK signaling pathway and is a novel potential biomarker for the diagnosis and prognosis of bladder cancer.

Poor prognosis of nucleophosmin overexpression in solid tumors: a meta-analysis

“…All 11 studies with a total of 997 patients were used immunohistochemistry method to detect the expression of NPM. The patients from China [ 3 , 14 , 25 – 29 ], Japan [ 30 ], Taiwan [ 31 , 32 ], Italy [ 15 ] were diagnosed with various tumors, including colon cancer, Ewing’s sarcoma, hepatocellular carcinoma, gastric cancer, ovarian serous cancer, colorectal carcinomas, glioma, astrocytoma, pancreatic ductal adenocarcinoma, bladder urothelial carcinoma. The main characteristics of these included studies are shown in Table 1 .…”

Multifunctional YY1 in Liver Diseases

“…The nucleolar phosphoprotein B23 is a positive regulator of cell proliferation and is markedly upregulated in and statistically correlated to poor prognosis of patients with various cancers, including bladder urothelial carcinoma, gastric cancer, smooth muscle tumors of the corpus uteri, and HCV-related HCC. [43][44][45][46] It has been reported that YY1 normally suppresses the B23 expression, possibly through the competition binding mechanism described in ►Fig. 1A.…”

“…7 YY1 gene expression can be stimulated by several growth factors, while antiproliferative signals tend to antagonize its expression. 6 In addition, analyses with GAL4 fusion proteins revealed the functional domains of YY1 proteins to reside in the C-terminus (amino acids [aa], 298-397), mediating its transcriptional repression ability, and the N-terminus (aa [43][44][45][46][47][48][49][50][51][52][53], mediating its potent transcriptional activation ability. 11 The list of target genes of YY1 is continuing to grow, and many of these represent key players in signaling pathways that regulate cancer development and progression, including such well-known factors as c-myc, c-fos, ERBB2, E1A, and p53.…”

NPM1 upregulates the transcription of PD-L1 and suppresses T cell activity in triple-negative breast cancer

“…NPM1 promotes metastasis in colon cancer and serves as a poor prognostic factor 23 . High expression of NPM1 is associated with tumorigenesis in bladder urothelial carcinoma 24 . Besides, downregulation of NPM1 increases radiation sensitivity in non-small-cell lung cancer (NSCLC) 25 .…”