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PAI-1 is a potential transcriptional silencer that supports bladder cancer cell activity

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE201518 | GEO | 2022/07/20

REPOSITORIES: GEO

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PAI-1 is a potential transcriptional silencer that supports bladder cancer cell activity.

Project description:The extracellular activity of Plasminogen activator inhibitor-1 (PAI-1) is well described, acting as an inhibitor of tissue plasminogen activator and urokinase-type plasminogen activator, impacting fibrinolysis. Recent studies have revealed a pro-tumorigenic role of PAI-1 in human cancers, via the regulation of angiogenesis and tumor cell survival. In this study, immunohistochemical staining of 939 human bladder cancer specimens showed that PAI-1 expression levels correlated with tumor grade, tumor stage and overall survival. The typical subcellular localization of PAI-1 is cytoplasmic, but in approximately a quarter of the cases, PAI-1 was observed to be localized to both the tumor cell cytoplasm and the nucleus. To investigate the potential function of nuclear PAI-1 in tumor biology we applied chromatin immunoprecipitation (ChIP)-sequencing, gene expression profiling, and rapid immunoprecipitation mass spectrometry to a pair of bladder cancer cell lines. ChIP-sequencing revealed that PAI-1 can bind DNA at distal intergenic regions, suggesting a role as a transcriptional coregulator. The downregulation of PAI-1 in bladder cancer cell lines caused the upregulation of numerous genes, and the integration of ChIP-sequence and RNA-sequence data identified 57 candidate genes subject to PAI-1 regulation. Taken together, the data suggest that nuclear PAI-1 can influence gene expression programs and support malignancy.

| S-EPMC9288475 | biostudies-literature

PAI-1 is a potential transcriptional silencer that supports bladder cancer cell activity [RNA-Seq]

2022-07-20 | GSE201517 | GEO

PAI-1 is a potential transcriptional silencer that supports bladder cancer cell activity [ChIP-Seq]

2022-07-20 | GSE201515 | GEO

PAI-1 is a potential transcriptional silencer that supports bladder cancer cell activity

Project description:PAI-1 is a potential transcriptional silencer that supports bladder cancer cell activity

| PRJNA832102 | ENA

PAI-1 is a potential transcriptional silencer that supports bladder cancer cell activity [ChIP-Seq]

Project description:PAI-1 is a potential transcriptional silencer that supports bladder cancer cell activity [ChIP-Seq]

| PRJNA832106 | ENA

PAI-1 is a potential transcriptional silencer that supports bladder cancer cell activity [RNA-Seq]

Project description:PAI-1 is a potential transcriptional silencer that supports bladder cancer cell activity [RNA-Seq]

| PRJNA832105 | ENA

Plasminogen activator inhibitor-2 (PAI-2) overexpression supports bladder cancer development in PAI-1 knockout mice in N-butyl-N- (4-hydroxybutyl)-nitrosamine- induced bladder cancer mouse model.

Project description:BackgroundAccumulating evidence suggests that plasminogen activator inhibitor-1 (PAI-1) plays an important role in bladder tumorigenesis by regulating cell cycle. However, it remains unclear whether and how inhibition of PAI-1 suppresses bladder tumorigenesis.MethodsTo elucidate the therapeutic effect of PAI-1 inhibition, we tested its tumorigenicity in PAI-1 knockout (KO) mice exposed to a known bladder carcinogen.ResultsPAI-1 deficiency did not inhibit carcinogen-induced bladder cancer in mice although carcinogen-exposed wild type mice significantly increased PAI-1 levels in bladder tissue, plasma and urine. We found that PAI-1 KO mice exposed to carcinogen tended to upregulate protein C inhibitor (PAI-3), urokinase-type plasminogen activator (uPA) and tissue-type PA (tPA), and significantly increased PAI-2, suggesting a potential compensatory function of these molecules when PAI-1 is abrogated. Subsequent studies employing gene expression microarray using mouse bladder tissues followed by post hoc bioinformatics analysis and validation experiments by qPCR and IHC demonstrated that SERPING1 is further downregulated in PAI-1 KO mice exposed to BBN, suggesting that SERPING1 as a potential missing factor that regulate PAI-2 overexpression (compensation pathway).ConclusionsThese results indicate that serpin compensation pathway, specifically PAI-2 overexpression in this model, supports bladder cancer development when oncoprotein PAI-1 is deleted. Further investigations into PAI-1 are necessary in order to identify true potential targets for bladder cancer therapy.

| S-EPMC7003426 | biostudies-literature

Potential Roles of IGF2BP3 in Bladder Cancer

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

2024-03-27 | GSE171024 | GEO

Identification of mir-342-3p functionally associated with transcriptional activity of MYC in lung cancer

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

2016-01-06 | E-GEOD-66760 | biostudies-arrayexpress

DNA methylation and expression profiling study for bladder cancer

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

2013-05-03 | E-GEOD-37817 | biostudies-arrayexpress