Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Landscape of genomic alterations in Indian Urinary Bladder cancer patients

ABSTRACT: Urinary bladder is an open system and is under constant carcinogenic insults leading to chromosomal aberrations. Chronic retention of urine in the bladder is considered one of the reasons for initiation of bladder cancer. Here, we have explored the genomic alterations in Indian BlCa patients by CGH-SNP microarray. The microarray data (n=10) revealed several alterations throughout the genome. Genomic regions like 2p25.3 [chr2: 3557810-3575411], 4p16.3 [chr4: 656211-657032], 7p22.3 [chr7: 990730-1000575], 10q26.13 [chr10: 123137874-123148372], 16q24.3 [chr16: 88835825-88837868], 17p11.2 [chr17: 17477220-17506264], 19q13.33 [chr19: 49861971-49862491], 20q13.33 [chr20: 63406442-63415195; 63415195-63495407] etc. were found to be frequently (≥40%) amplified among the 10 BlCa samples. Regions like 2q37.2 [chr2: 235384329- 235479250], 8p23.3-11.21 [chr 8: 236477- 39291988], 10q21.1-26.3 [chr 10: 55309072- 133391562], 11p12 [chr 11: 37327799- 38803561], 12q24.31-24.33 [chr 12: 128515048- 133047983], and 13q13.3-34 [chr 13: 35583974- 113996673] etc. are identified as common deletion (30%). Chromosomal regions like 2p25.3, 16q24.3 and 20q13.33 showed the highest frequency of amplification (70%), whereas 2q37.2, 10q21.1, 11p12, 11q22.3, etc. showed the highest frequency of deletion (30%). Chromosome 7, 15 and 21 showed the least alterations in these samples. Almost a complete loss in 8p chromosomal arm (8p23.1-11.22), chromosome 11q (11q14.1-25) and chromosome 13 (13q13.3-34) were found in 30% of samples, signifying their plausible role in development of BlCa.

ORGANISM(S): Homo sapiens

PROVIDER: GSE122514 | GEO | 2020/11/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Unveiling the association between HMG-CoA reductase inhibitors and bladder cancer

Project description:This study utilized Mendelian randomization (MR) analysis and genome-wide association study (GWAS) data to investigate the association between commonly prescribed drugs and bladder cancer (BLCA) risk. Our results revealed that HMGCR inhibitors, specifically simvastatin, are significantly associated with a reduced BLCA risk. We further showed that simvastatin could significantly inhibit BLCA proliferation and epithelial-mesenchymal transition in animal models, with transcriptomic data identifying several associated pathways. Higher levels of HMGCR were linked with BLCA development and progression, and certain blood lipids, such as lipoprotein particles and VLDL cholesterol, might influence BLCA risk. These findings suggested that HMGCR inhibitors, particularly simvastatin, could be potential treatment options or adjuvant therapies for BLCA. Meanwhile, RhoB is a key protein involved in the regulation of bladder cancer cell metastasis by simvastatin. Therefore, we tested the changes of key genes in bladder cancer cells after simvastatin (HMGCR inhibitor) treatment and overexpression of RhoB, respectively, using RNA sequencing.

2024-09-08 | GSE270394 | GEO

Chromosomal aberrations of human bladder cancer cell lines

Project description:In order to identify putative targets in human bladder cancer (BC) cell lines, a survey of parallel chromosomal alterations and gene expression studies in 5 BC cell lines were performed using array-CGH and microarray techniques. Predominantly gained loci were observed at 1q21.3, 8q24.2, 8q24.3, 11q13.3, and 20q13.33 in four or more of the cell lines. The focus was on the typical gain locus of 8q24.3, which has not been studied in detail for BC.

2010-01-05 | GSE19714 | GEO

Mevalonate pathway inhibition affects bladder cancer metastasis

Project description:Metastasis is an important factor affecting the prognosis and survival of bladder cancer (BLCA) patients. Our previous study found that the mevalonate pathway is associated with the migratory ability of BLCA cells, but the exact mechanism is unclear. Here, we found that BLCA patients with mevalonate pathway activation had a poorer prognosis. Inhibition of the mevalonate pathway (FDPS knockdown, simvastatin or zoledronic acid) significantly reduced the migratory ability of BLCA cells. Therefore, we tested the changes of key genes after knocking down the key enzymes of the mevalonate pathway, FDPS and SQLE1, and the transcription factor YY1 in bladder cancer cells using RNA sequencing.

2024-09-08 | GSE252007 | GEO

EGFR activity addiction facilitates anti-ERBB based combination treatment of squamous bladder cancer

Project description:Recent findings suggested a benefit of anti-EGFR therapy for basal-like muscle invasive bladder cancer (MIBC). However, impact on bladder cancer with substantial squamous differentiated (Sq-BLCA) and especially pure squamous cell carcinoma (SCC) remains unknown. Therefore, we comprehensively characterized pure and mixed Sq-BLCA (n=125) on genetic and protein expression level, and performed functional pathway and drug-response analyses with cell line models and isolated primary SCC (p-SCC) cells of the human urinary bladder. We identified abundant EGFR expression in 95% of Sq-BLCA without evidence for activating EGFR mutations. Both SCaBER and p-SCC cells were sensitive to EGFR tyrosine kinase inhibitors (TKIs: erlotinib and gefitinib). Combined treatment with anti-EGFR TKIs and varying chemotherapeutics led to a concentration-dependent synergism in SCC cells according to the Chou-Talalay method. In addition, siRNA knockdown of EGFR impaired SCaBER viability suggesting a putative ‘‘Achilles heel’’ of Sq-BLCA. The observed effects seem Sq-BLCA-specific since non-basal urothelial cancer cells were characterized by poor TKI sensitivity associated with a short-term feedback response by upregulating EGFR and ERBB3 expression. Hence, our findings give novel insights into a crucial, Sq-BLCA-specific role of the ERBB signaling pathway proposing improved effectiveness of combined anti-EGFR and chemotherapeutic regimens in squamous bladder cancers with wild-type EGFR-overexpression.

2023-03-12 | GSE146975 | GEO

In-depth protein profiling of cytology samples in urothelial carcinoma

Project description:Urine cytologic examination is a widely used primary pathologic screening test in the diagnosis of bladder urothelial carcinoma (BLCA), however the low diagnostic accuracy remains challenging. We conducted high-throughput proteome on ten pairs of BLCA and benign urothelial lesion (BUL) to identify a supportive proteomic marker as an ancillary test in liquid based cytology (LBC).

2018-07-04 | PXD006805 | Pride

ACAT1 promotes bladder tumorigenesis by inducing cell cycle via AKT/GSK3β/c-Myc signaling pathway

Project description:Acetyl-CoA acetyltransferase 1 (ACAT1) played a key role in regulating gene expression and tumorigenesis. Nevertheless, the biological function of ACAT1 in bladder cancer (BLCA) has yet to be elucidated. This study aimed to elucidate the bioinformatics features and biological functions of ACAT1 in BLCA. Here, we demonstrate for the first time that ACAT1 is elevated in BLCA tissues, correlating with specific clinicopathological features and an unfavorable prognosis for survival in BLCA patients. ACAT1 emerged as an independent risk factor in BLCA. Phenotypically, ACAT1 knockdown inhibited the proliferation and migration of BLCA cells both in vivo and in vitro, whereas ACAT1 overexpression yielded the opposite phenotype. Mechanistically, ACAT1 enhances BLCA cells proliferation by activating cell cycle through AKT/GSK3β/c-Myc signaling pathway. In conclusion, this study identifies ACAT1 as an oncogene in BLCA, demonstrating its capability to promote proliferation and metastasis of BLCA. This suggests that ACAT1 may serve as a potential molecular target for the diagnosis and treatment of BLCA.

2024-06-12 | GSE248825 | GEO

A positive feedforward circuit shaped by DLGAP5 and E2F1 triggers bladder cancer progression

Project description:Bladder cancer (BLCA) is a highly prevalent malignancy on a global scale, characterized by significant tumor heterogeneity. The investigation of molecular mechanisms that can be leveraged for the management of aggressive BLCA represents a particularly pertinent objective.DLGAP5 is mitosis-related protein widely existed in eukaryotic cells. The molecular mechanism of DLGAP5 in bladder cancer is still not clear, despite its role in tumorigenesis. Bladder cancer tissues exhibit a noteworthy increase in DLGAP5 expression, compared to normal bladder tissues. Furthermore, the expression of DLGAP5 shows a positive correlation with the clinical stage of the tumor and a negative impact on the prognosis. Cell proliferation and migration are significantly impacted by alterations in DLGAP5 expression, as demonstrated by in vitro and in vivo experiments. Further investigation reveals that DLGAP5 regulated E2F1 protein stability via USP11 deubiquitinase activity, and DLGAP5 is a direct target of E2F1. DLGAP5-E2F1 forms a positive feedback loop and influences the efficacy of BLCA progression. Collectively, DLGAP5 could potentially serve as a new therapeutic target for the treatment of bladder cancer.

2023-12-31 | GSE241523 | GEO

Melatonin inhibited tumorigenesis of bladder cancer via suppressing PPARγ/ENO1 mediated glycolysis

Project description:Bladder cancer (BLCA) is one of the most malignant human cancers in the world. The increasingly prominent phenomenon of chemoresistance has become an essential obstacle to clinical treatment for BLCA, and there is an urgent need to explore novel drugs to improve the current clinical status. Melatonin is a well-known natural hormone that showed a potential anti-cancer effect in multiple human cancers. In our study, we comprehensively explored the inhibitory effect of melatonin on BLCA and found that it could suppress the glycolysis process in BLCA cells. Moreover, we discovered that the ninth step enzyme ENO1 of glycolysis was the downstream effector of melatonin and could be a predictive biomarker of BLCA patients.

2022-09-06 | GSE212599 | GEO

Label-free global proteome profiling of European American and African American bladder tumor patients.

Project description:Bladder cancer (BLCA) mortality is higher in African American (AA) patients compared to their European American (EA) counterparts, but the molecular mechanism underlying differences are unknown. . Thus, we performed proteomics analysis of AA and EA BLCA and identified higher mitochondrial OXPHOS specifically through complex I activation in AA BLCA.

2024-08-08 | MSV000095559 | MassIVE

DNA polymerase POLD1 promotes proliferation and metastasis of bladder cancer by stabilizing MYC

Project description:Hitherto, most studies on POLD1 have mainly focused on the effect of POLD1 inactivation mutation in tumors. Nonetheless, the mechanism underlying high POLD1 expression in tumorigenesis remains elusive. Herein, we substantiated the pro-carcinogenic role of POLD1 in bladder cancer (BLCA) and found that POLD1 expression is related to malignancy and prognosis of BLCA. Next, we demonstrated that POLD1 could promote proliferation and metastasis of BLCA via MYC. Mechanistically, we demonstrated that POLD1 was able to stabilize MYC in a manner independent of DNA polymerase activity. POLD1 attenuated the FBXW7-mediated ubiquitination degradation of MYC by directly binding to the MYC homology box 1 domain competitively with FBXW7. Moreover, we found that POLD1 can form a complex with MYC to promote the transcriptional activity of MYC. MYC could also transcriptionally activate POLD1, forming a POLD1-MYC positive feedback loop to enhance the pro-carcinogenic effect of POLD1-MYC on BLCA. Overall, our study suggests a novel MYC-driven mechanism for BLCA, and POLD1 has the potential as a biomarker for BLCA.

2023-03-29 | PXD040806 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data