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The Androgen Receptor Directly Regulates CD44 Expression in Androgen Sensitive Bladder Cancer [gene expression]

ABSTRACT: The Androgen Receptor Directly Regulates CD44 Expression in Androgen Sensitive Bladder Cancer [gene expression]

PROVIDER: PRJNA622580 | ENA |

REPOSITORIES: ENA

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The Androgen Receptor Directly Regulates CD44 Expression in Androgen Sensitive Bladder Cancer

Project description:The Androgen Receptor Directly Regulates CD44 Expression in Androgen Sensitive Bladder Cancer

| PRJNA622576 | ENA

The Androgen Receptor Directly Regulates CD44 Expression in Androgen Sensitive Bladder Cancer [ChIP-seq]

Project description:The Androgen Receptor Directly Regulates CD44 Expression in Androgen Sensitive Bladder Cancer [ChIP-seq]

| PRJNA622581 | ENA

The Androgen Receptor Directly Regulates CD44 Expression in Androgen Sensitive Bladder Cancer [gene expression]

Project description:To study androgen receptor transcriptomic activation in the presence of androgen in bladder cancer cell lines. A uniquely derived AR expressing clone of the bladder cancer cell line UMUC3 was derived and validated prior to microarray experiments. Microarrays were used to determine the overall expression changes in repsonse to treatment with synthetic androgen. Evaluation of genes associated with androgen receptor stimulation were used for focused analysis when combined with ChIP-seq data.

2021-03-21 | GSE147938 | GEO

The Androgen Receptor Directly Regulates CD44 Expression in Androgen Sensitive Bladder Cancer [ChIP-seq]

Project description:To study androgen receptor transcriptomic activation in the presence of androgen in bladder cancer cell lines. A uniquely derived AR expressing clone of the bladder cancer cell line UMUC3 was derived and validated prior to ChIP-seq experiments. Androgen receptor chromatin immunoprecipitation (AR ChIP-seq) was used to determine the overall expression changes in repsonse to treatment with synthetic androgen. Evaluation of genes associated with androgen receptor stimulation were used for focused analysis when combined with microarray data.

2021-03-21 | GSE147939 | GEO

The Androgen Receptor Directly Regulates CD44 Expression in Androgen Sensitive Bladder Cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-03-21 | GSE147940 | GEO

Androgen Receptor Regulates CD44 Expression in Bladder Cancer.

Project description: Not available

| S-EPMC8782536 | biostudies-literature

Androgen-sensitive glycomembrane protein expression in LNCaP prostate tumor cells

Project description:Aberrant androgen receptor (AR)-mediated transcription is a critical driver in progression of human prostate cancer. It's known that different doses of androgens can elicit differential transcriptional and proliferative responses in prostate-tumor cells. Here, we set out to examine the androgenic regulation of glycoprotein expression in the membrane fraction of prostate-tumor cells that could serve as mediators or markers of androgen-induced proliferative responses observed in prostate-tumor cells. A bioanalytical workflow involving lectin-affinity chromatography and label-free quantitative mass spectrometry was used to identify androgen-sensitive glycomembrane protein expression associated with androgen-mediated proliferation. This study would facilitate the identification of surface membrane proteins involved in androgen-mediated proliferation and provide potential therapeutic targets in the detection treatment of proliferation prostate-tumors.

2022-03-01 | PXD002913 | Pride

Urinary Glycoproteomic profiling of Non-Muscle Invasive and Muscle Invasive Bladder Carcinoma Patients reveals distinct N-glycosylation pattern of CD44, MGAM and GINM1

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.

2020-09-10 | PXD020078 | Pride

Enzalutamide inhibits proliferation of gemcitabine-resistant bladder cancer cells with increased androgen receptor expression

Project description:Advanced bladder cancer is treated mainly with gemcitabine and cisplatin, but most patients eventually become resistance to these chemotherapeutic agents. Androgen receptor (AR) signaling has been implicated in bladder cancer as well as other types of cancer including prostate cancer. In the present study, we showed the expression and role of AR in gemcitabine-resistant bladder cancer cells and examined the potential of enzalutamide, an AR inhibitor, as a therapeutic for the chemoresistance. First of all, we established gemcitabine-resistant T24 cells (T24GR) from T24 bladder cancer cells and performed gene expression profiling and network analysis, which revealed increased AR expression and AR-related gene network in T24GR cells. Quantitative RT-PCR and Western blot analysis confirmed increased expression of AR in T24GR cells compared with parental T24 cells, which was associated with more potent transcriptional activity of AR in T24GR cells. The number of AR gene copy in T24GR cells was twice as many as that of T24 cells. Knockdown of AR expression by siRNA resulted in inhibition of proliferation of T24GR cells. Cell culture in charcoal-stripped serum and treatment with enzalutamide also inhibited growth of T24GR cells, which was accompanied by cell cycle arrest. Lastly, the AR transcriptional activity was found to be reduced in T24GR cells by enzalutamide treatment. Our results suggest that blockade of AR signaling by enzalutamide might be effective for patients with advanced gemcitabine-resistant bladder cancer with increased AR expression.

2016-11-30 | GSE77883 | GEO

Evaluation of gene expression between CD44+ and CD44- cells in colonospheres

Project description:To identify genes that are differentially expressed between CD44+ and CD44- cells in colonospheres, we have employed whole genome microarray expression profiling as a discovery platform. Colonospheres from four colon cancer patients were sorted into CD44+ and CD44- cells using the FACS Aria II Cell Sorter, and total RNA extracted from the cells were labeled with Cy3 and used for microarray analyses with Agilent Whole Human Genome Oligo Microarrays. Gene expression in fluorescence-activated cell-sorted CD44+ and CD44- cells derived from four colon cancer patients was measured.

2012-12-07 | E-GEOD-38706 | biostudies-arrayexpress

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