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KMT9 is an actionable target in muscle-invasive bladder cancer

ABSTRACT: KMT9 is an actionable target in muscle-invasive bladder cancer

PROVIDER: PRJNA1074717 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27918800_1.fastq.gz	Fastqsanger.gz
	SRR27918800_2.fastq.gz	Fastqsanger.gz
	SRR27918801_1.fastq.gz	Fastqsanger.gz
	SRR27918801_2.fastq.gz	Fastqsanger.gz
	SRR27918802_1.fastq.gz	Fastqsanger.gz

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KMT9 is an actionable target in muscle-invasive bladder cancer

Project description:Novel treatment modalities are imperative for the challenging management of muscle-invasive and metastatic BC to improve patient survival rates. The recently identified lysine methyltransferase (KMT) 9, an obligate heterodimer composed of KMT9α and KMT9β, regulates the growth of various types of tumors such as prostate, lung and colon cancer. While overexpression of KMT9α was previously observed to be associated with aggressive basal-like MIBC in an analysis of patients’ tissue samples, a potential functional role of KMT9 in this type of cancer has not been investigated to date. In this study, we show that KMT9 regulates proliferation and migration of various MIBC cell lines with different genetic mutations. KMT9α depletion results in differential expression of genes involved in the regulation of the cell cycle, cell adhesion and migration. Reduced cell proliferation upon KMT9α depletion is also observed in Pten/Trp53 knockout bladder tumor organoids, which cannot be rescued with an enzymatically inactive KMT9α mutant. In accordance with the idea that the catalytic activity of KMT9 is required for the control of cellular processes in MIBC, a recently developed small molecule inhibitor of KMT9 (KMI169) also impairs cancer cell proliferation. Since KMT9α depletion also restricts the growth of xenografts in mice, our data suggest that KMT9 is an actionable novel therapeutic target for the treatment of MIBC.

2024-05-01 | GSE255344 | GEO

Comparison of gene expression profiling of human non-muscle invasive bladder cancer and muscle invasive bladder cancer

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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Project description:Gene expression profiling of 82 human non-muscle invasive bladder carcinoma and 4 normal bladder samples, for a total of 86 tissues. A Cartes d‚àö‚â†Identite des Tumeurs (CIT) study from the 'Institut Curie' and the french 'Ligue Nationale Contre le Cancer' (http://cit.ligue-cancer.net/).

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Project description:Although non muscle-invasive bladder cancer can be treated successfully by surgical resection, there is a high rate of recurrence, which frequently develops into an invasive form of cancer. Due to the lack of marker molecules to predict recurrence, it is currently recommended that after resection each patient is screened via cystoscopy at least twice a year. This results in a psychic burden to the patient and substantial economic costs to the health care system. Using antibody microarrays targeting 724 different cancer-related proteins, we studied protein profiles of patients with and without recurrence. The analysis revealed 255 proteins of differential abundance. Most are involved in the regulation and execution of apoptosis and cell proliferation. For prognosis, a signature of 20 proteins was determined that predicts bladder cancer recurrence with 100% sensitivity and 80% specificity. As a measure of overall accuracy, the area under the curve (AUC) value was found to be 90%. This is well within a clinically relevant window of quality and should support decision making about the stringency of surveillance or even different treatment options.

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Project description:This RNA-sequencing cohort includes 52 Non-muscle Invasive Bladder cancer (NMIBC) samples and 6 Muscle Invasive Bladder cancer (MIBC) samples.

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Project description:Clinical management of bladder carcinomas (BC) remains a major challenge and demands comprehensive multi-omics analysis for better stratification of the disease. Identification of patients on risk requires identification of signatures predicting prognosis risk of the patients. Understanding the molecular alterations associated with the disease onset and progression could improve the routinely used diagnostic and therapy procedures. In this study, we investigated the aberrant changes in N-glycosylation pattern of proteins associated with tumorigenesis as well as disease progression in bladder cancer. We integrated and compared global N-glycoproteomic and proteomic profile of urine samples from bladder cancer patients at different clinicopathological stages (non-muscle invasive and muscle-invasive patients (n=5 and 4 in each cohort)) with healthy subjects (n=5) using SPEG method. We identified 635 N-glycopeptides corresponding to 381 proteins and 543 N-glycopeptides corresponding to 326 proteins in NMIBC and MIBC patients respectively. Moreover, we identified altered glycosylation in 41 NMIBC and 21 MIBC proteins without any significant change in protein abundance levels. In concordance with the previously published bladder cancer cell line N-glycoproteomic data, we also observed dysregulated glycosylation in ECM related proteins. Further, we identified distinct N-glycosylation pattern of CD44, MGAM and GINM1 between NMIBC and MIBC patients, which may be associated with disease progression in bladder cancer. These aberrant protein glycosylation events would provide a novel approach for bladder carcinoma diagnosis and further define novel mechanisms of tumor initiation and progression.

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