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Cell-intrinsic tumorigenic functions of PPARg in bladder urothelial carcinoma

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE166803 | GEO | 2021/02/22

REPOSITORIES: GEO

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Cell-intrinsic tumorigenic functions of PPARg in bladder urothelial carcinoma [ChIP-seq]

Project description:PPARg promotes UC progression through cell-autonomous mechanisms linked to sonic hedgehog (SHH) signaling.

2021-02-22 | GSE166802 | GEO

Cell-intrinsic tumorigenic functions of PPARg in bladder urothelial carcinoma [RNA-seq]

Project description:PPARg promotes UC progression through cell-autonomous mechanisms linked to sonic hedgehog (SHH) signaling.

2021-02-22 | GSE166801 | GEO

Cell-Intrinsic Tumorigenic Functions of PPARγ in Bladder Urothelial Carcinoma.

Project description:The role of PPAR gamma (PPARγ) has been well characterized in the developmental process of adipogenesis, yet its aberrant expression patterns and functions in cancer subtypes are less understood. Although PPARγ has been recently demonstrated to play non-cell-autonomous roles in promoting bladder urothelial carcinoma (UC) progression, underlying mechanisms of the cell-intrinsic oncogenic activity remain unknown. Here, we report robust expression and nuclear accumulation of PPARγ in 47% of samples of patients with UC, exceeding mRNA expression patterns published by The Cancer Genome Atlas. In vitro assays revealed for the first time that treatment of UC cells with PPARγ inverse agonist or PPARG knockout by CRISPR-Cas9 reduces proliferation, migration, and invasion of multiple established UC cell lines, most strongly in those characterized by PPARG genomic amplification or activating mutations of RXRA, the obligate heterodimer of PPARγ. Through genome-wide approaches including chromatin immunoprecipitation sequencing and RNA sequencing, we define a novel set of PPARγ-regulated genes in UC, including Sonic Hedgehog (SHH). Similar to PPARγ, genetic inhibition of SHH reduces proliferation and motility. Finally, we demonstrate the PPARγ dependency of UC tumors in vivo by genetic and pharmacologic PPARγ inhibition in subcutaneous xenografts. Collectively, our data indicate that PPARγ promotes UC progression in a subset of patients, at least in part, through cell-autonomous mechanisms linked to SHH signaling. IMPLICATIONS: Genome-wide analysis of DNA-binding sites for oncogenic factor PPARγ revealed SHH as a novel downstream target involved in UC progression, providing important insight into the tumorigenic nature and molecular mechanism of PPARγ signaling in UC.

| S-EPMC8026526 | biostudies-literature

Cell-intrinsic tumorigenic functions of PPARg in bladder urothelial carcinoma

Project description:Cell-intrinsic tumorigenic functions of PPARg in bladder urothelial carcinoma

| PRJNA701983 | ENA

Cell-intrinsic tumorigenic functions of PPARg in bladder urothelial carcinoma [ChIP-seq]

Project description:Cell-intrinsic tumorigenic functions of PPARg in bladder urothelial carcinoma [ChIP-seq]

| PRJNA702004 | ENA

Cell-intrinsic tumorigenic functions of PPARg in bladder urothelial carcinoma [RNA-seq]

Project description:Cell-intrinsic tumorigenic functions of PPARg in bladder urothelial carcinoma [RNA-seq]

| PRJNA702003 | ENA

The UBC-40 Urothelial Bladder Cancer Cell Line Index

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-06-19 | E-GEOD-64573 | biostudies-arrayexpress

DNA copy number alterations and PPARG amplification in a patient with multifocal bladder urothelial carcinoma.

Project description:BackgroundBladder cancer is the seventh most common cancer worldwide and over 90% are transitional cell carcinoma (TCC). At the first time of diagnosis at least 70% of TCC present as superficial bladder cancer. Because the clinical outcome of superficial bladder tumors is relatively unpredictable, there is a pressing need to identify markers that may predict tumor recurrence and progression and new treatment strategies.Case presentationWe present a unique case of a 67-year old male who underwent total cystectomy after repeated trans-urethral resections of the bladder for multifocal non-muscle invasive bladder cancer. The first and the third tumor were diagnosed as high grade non-infiltrating (HGNI), while the second as carcinoma in situ (CIS). We performed both array comparative genomic hybridization and a targeted chromosomal profile by UroVysion in order to detect copy number variations (CNVs) that may be involved with tumor recurrence and progression. The overall data from this study provide new evidence for the monoclonal origin of urothelial tumor multifocality as several genetic changes were found in different tumors of the same patient. From the analysis of shared CNVs two gained regions emerged at 3p25.2 and 12q23.2, including PPARG and ASCL1 genes, respectively. The copy number level of these genes would seem inversely mutually correlated and highly dependent on histological grade, because the highest level of amplification at 3p25.2 was evidenced in the two HGNI samples, while the highest level of copy number gain at 12q23.2 was reported in the CIS.ConclusionWe provide new evidence on the role of PPARG in initiation and maintenance of bladder cancer. For the first time we also suggest a possible explanation for the elevated expression of PPARG in this type of tumor through a focal high level amplification at 3p25.2. Furthermore, a new gene, ASCL1, emerged as a potential candidate to assist PPARG in bladder carcinogenesis.

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The UBC-40 Urothelial Bladder Cancer Cell Line Index

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

2015-06-19 | GSE64573 | GEO

RNA sequencing of chemotherapy-resistant muscle-invasive urothelial bladder cancer

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

2020-03-26 | GSE145140 | GEO