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Nucleocytoplasmic β‐Catenin expression contributes to neuroendocrine differentiation in muscle invasive bladder cancer

ABSTRACT: Nucleocytoplasmic β‐Catenin expression contributes to neuroendocrine differentiation in muscle invasive bladder cancer

PROVIDER: PRJNA1063740 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27497254_1.fastq.gz	Fastqsanger.gz
	SRR27497254_2.fastq.gz	Fastqsanger.gz
	SRR27497255_1.fastq.gz	Fastqsanger.gz
	SRR27497255_2.fastq.gz	Fastqsanger.gz
	SRR27497256_1.fastq.gz	Fastqsanger.gz

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Nucleocytoplasmic β‐Catenin expression contributes to neuroendocrine differentiation in muscle invasive bladder cancer

Project description:Muscle invasive bladder cancer (MIBC) is highly heterogeneous, both at the molecular level and in terms of clinical progression. Several molecular classifications have been proposed to understand this heterogeneity and contribute to diagnosis and treatment. Although the neuroendocrine-like subtype is the most aggressive and exhibits the worst survival rate when compared to other subtypes, molecular mechanisms underlying neuroendocrine differentiation have not yet been understood. The nuclear localization of β-catenin is known to be associated with the activation of the Wnt/β-catenin pathway, and it is linked to disease progression and aggressiveness in various cancer types. To decipher the mechanisms underlying the neuroendocrine differentiation of bladder cancer, we determined β-catenin expression profiles of 169 T2-stage primary MIBC samples. Immunohistochemistry analysis revealed increased expression of the most widely used NE markers SYP, CGA, and CD56 in β-catenin positive MIBC tumors. As a result of our transcriptomic analysis, we observed higher expression of neuroendocrine differentiation-related genes, and lower expression of basal differentiation and urothelial differentiation-related genes in β-catenin positive MIBC tumors. Furthermore, we applied a molecular consensus classifier to β-catenin positive and negative samples, and the NE score was significantly higher in β-catenin positive MIBC compared to others. By comparing transcriptome proﬁles, we reveal that β-catenin positive MIBC harbor unique gene modules and gene expression profiles that are divergent from the β-catenin negative MIBC. GO term and KEGG pathway analyses showed that various neurogenesis-related pathways as well as regulation of gene expression and chromatin remodeling were significantly enriched at β-catenin positive MIBC. Our results collectively revealed that β-catenin expression contributes to neuroendocrine differentiation of bladder cancer.

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Project description:Neuroendocrine bladder cancer is an aggressive variant of bladder cancer with significant metastatic potential and high risk of mortality. Diagnosis of these tumors is currently dependent on morphological criteria and staining for neuroendocrine markers. Using machine learning and multiple validation cohorts in different clinical settings, we developed a model that identifies tumors with transcriptomic profiles consistent with NE bladder cancers with an absence of NE features by morphological criteria. Early and accurate identification of these patients by genomic analysis may improve outcomes through treatment intensification and adaptation of standard treatment regimens.

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Molecular characterizaion of neuroendocrine-like bladder cancer

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Project description:The biological behaviors, clinical treatment, prognosis of nonmuscle-invasive bladder cancers (NMIBCs) and muscle-invasive bladder cancers (MIBCs) are distinct. Therefore, we performed high-through microarray screening of mRNA expression in 30 bladder tumors, to filter out some of the differential expression genes in NMIBCs and MIBCs.A total of 11 Genes in MIBCs versus in NMIBCs were considered differentially transcribed if they were transcribed ≤2.0 fold change and p<0.001 by unpaired T-test, including 9 up-regulated genes and 2 down-regulated genes in MIBCs (NR4A2, PLK3, CYR61, APOLD1, C13ORF33, LIG4, RBMS3, PCK2, AK098422, HSD17B3, RTN4). These candidate genes were validated in further and provide further insight into the discovery of new putative markers to identify MIBCs preoperatively.

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2015-03-10 | E-GEOD-66682 | biostudies-arrayexpress

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Project description:Three subtypes of small cell/neuroendocrine bladder cancers (SCBCs) were identified: ASCL1, NEUROD1, and POU2F3. These subtypes are with neuroendocrine (NE) level, immune signature, and antibody-drug conjugate (ADC) target implications.

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Project description:Although the pathological hallmark of amyotrophic lateral sclerosis (ALS) is the nucleocytoplasmic mislocalisation of RNA binding proteins (RBPs), such as TDP-43 and FUS, the nucleocytoplasmic distribution of mRNA remains uncharacterised. Here, we used subcellular fractionation with RNA sequencing to assess nucleocytoplasmic mRNA localisation in human induced pluripotent stem cell-derived motor neurons (iPSNs) from ALS patients with TARDBP mutations, VCP mutations, and controls with VCP mutations isogenically knocked in with CRISPR/Cas9. In each mutant group, we found substantial nucleocytoplasmic mRNA redistribution, particularly in transcripts involved in protein binding. Redistributed transcripts in ALS iPSNs were enriched in protein-coding biotypes, exhibited longer lengths, and had enhanced interactions with RBPs, including TDP-43 and FUS. Treatment with the VCP D2 ATPase domain inhibitor ML240 partially restored nucleocytoplasmic mRNA redistribution not only in VCP mutants but also in TARDBP mutant iPSNs.

2023-07-21 | GSE214017 | GEO

TET1 is a tumour suppressor that inhibits bladder cancer progression

Project description:Ten-Eleven Translocation 1 (TET1) is a member of methylcytosine dioxygenase, which catalyse 5-methylcytosine (5-mC) to 5-hydroxymethylcytosine (5-hmC) that promote the demethylation process. The diminished expression of TET1 protein and 5-hmC in many tumors indicate a critical role for the maintenance of cell stability. However, role of TET1 in bladder cancer development remains unclear. Here we found that TET1 expression was downregulated in bladder cancer tissues compared with normal urothelium and was inversely related to patient overall survival. TET1 silencing in bladder cancer cells increase proliferation and inhibited cell migration and invasion while its re-expression inhibits their proliferation and the growth of tumor xenografts. Furthermore, we found that TET1 binds to the promoter of the TSG to maintain its hypomethylated which interacts with β-catenin and suppress its nuclear translocation, thus inhibiting β-catenin transcriptional activity and downstream genes. In conclusion, TET1 acts as a tumor suppressor gene in bladder cancer cells by suppressing β-catenin signaling. This study may facilitate efforts to therapeutic strategy for patients with bladder cancer.

2020-06-16 | GSE137646 | GEO

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