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Circular RNA circRIMS1 acts as a sponge of miR-433-3p to promote bladder cancer progression by regulating CCAR1 expression (circRNA)

ABSTRACT: Circular RNA circRIMS1 acts as a sponge of miR-433-3p to promote bladder cancer progression by regulating CCAR1 expression (circRNA)

PROVIDER: PRJNA631252 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11735813_1.fastq.gz	Fastqsanger.gz
	SRR11735813_2.fastq.gz	Fastqsanger.gz
	SRR11735814_1.fastq.gz	Fastqsanger.gz
	SRR11735814_2.fastq.gz	Fastqsanger.gz
	SRR11735815_1.fastq.gz	Fastqsanger.gz

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Circular RNA circRIMS1 acts as a sponge of miR-433-3p to promote bladder cancer progression by regulating CCAR1 expression (circRNA)

Project description:Background: Circular RNAs (circRNAs), a subclass of noncoding RNAs, have been reported to be involved in the progression of various diseases. However, the exact role of circRIMS1, also termed hsa_circ_0132246, in human bladder cancer remains to be discovered. Methods: By performing RNA-seq comparing bladder cell lines and normal uroepithelial cells, circRIMS1 was selected as the research object. We further verified by qRT-PCR that circRIMS1 was upregulated in bladder cancer tissue and cell lines. Proliferation, colony formation, Transwell migration, Matrigel invasion, apoptosis, western blotting and in vivo tumorigenesis and metastasis assays were utilized to evaluate the roles of circRIMS1, miR-433-3p and CCAR1. For mechanistic investigation, RNA pull-down, fluorescence in situ hybridization (FISH) and luciferase reporter assay confirmed the binding of circRIMS1 with miR-433-3p. Results: CircRIMS1 was significantly upregulated in bladder cancer and circRIMS1 expression was associated with the pathological stage and histological grade of bladder cancer. Inhibition of circRIMS1 suppressed the proliferation, migration and invasion of bladder cancer cells in vitro and in vivo, while overexpression of circRIMS1 exerted the opposite effects. Moreover, the circRIMS1/miR-433-3p/CCAR1 regulatory axis was confirmed to be responsible for the biological functions of circRIMS1. Conclusions: CircRIMS1 acts as a tumor promoter in bladder cancer to enhance tumor growth, migration and invasion via the miR-433-3p/CCAR1 regulatory axis, which provides a new therapeutic target and a novel biomarker in bladder cancer. Keywords: CircRIMS1, Bladder cancer, miR-433-3p, CCAR1, Progression, Metastasis

2020-05-09 | GSE150142 | GEO

Circular RNA circRIMS1 acts as a sponge of miR-433-3p to promote bladder cancer progression by regulating CCAR1 expression (mRNA)

2020-05-09 | GSE150143 | GEO

Circular RNA circRIMS1 acts as a sponge of miR-433-3p to promote bladder cancer progression by regulating CCAR1 expression

Project description:Circular RNA circRIMS1 acts as a sponge of miR-433-3p to promote bladder cancer progression by regulating CCAR1 expression

| PRJNA631251 | ENA

Circular RNA circRIMS1 acts as a sponge of miR-433-3p to promote bladder cancer progression by regulating CCAR1 expression (mRNA)

Project description:Circular RNA circRIMS1 acts as a sponge of miR-433-3p to promote bladder cancer progression by regulating CCAR1 expression (mRNA)

| PRJNA631256 | ENA

Circular RNA circRIMS1 Acts as a Sponge of miR-433-3p to Promote Bladder Cancer Progression by Regulating CCAR1 Expression.

Project description:Circular RNAs (circRNAs), a subclass of noncoding RNAs, are reportedly involved in the progression of various diseases. However, the exact role of circRIMS1, also termed hsa_circ_0132246, in human bladder cancer remains unknown. By performing RNA sequencing comparing bladder cell lines and normal uroepithelial cells, circRIMS1 was selected as a research object. We further verified by qRT-PCR that circRIMS1 is upregulated in both bladder cancer tissue and cell lines. Proliferation, colony-formation, Transwell migration, invasion, apoptosis, western blotting, and in vivo experiments were utilized to clarify the roles of circRIMS1, microRNA (miR)-433-3p, and cell cycle and apoptosis regulator 1 (CCAR1). For mechanistic investigation, RNA pulldown, fluorescence in situ hybridization (FISH), and luciferase reporter assay confirmed the binding of circRIMS1 with miR-433-3p. Inhibition of circRIMS1 suppressed the proliferation, migration, and invasion of bladder cancer cells both in vitro and in vivo. Moreover, the circRIMS1/miR-433-3p/CCAR1 regulatory axis was confirmed to be responsible for the biological functions of circRIMS1. Taken together, our research demonstrated that circRIMS1 promotes tumor growth, migration, and invasion through the miR-433-3p/CCAR1 regulatory axis, representing a potential therapeutic target and biomarker in bladder cancer.

| S-EPMC7658378 | biostudies-literature

Circular RNA circRIMS1 acts as a sponge of miR-433-3p to promote bladder cancer progression by regulating CCAR1 expression

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

2020-05-09 | GSE150145 | GEO

CircRNA hsa_circ_0008500 Acts as a miR-1301-3p Sponge to Promote Osteoblast Mineralization by Upregulating PADI4.

Project description:Circular RNAs (circRNAs) are regarded as pivotal regulators in bone metabolism. However, the role of circRNAs in osteoblast mineralization remains largely unknown. Herein, we explored the expression profiles of circRNAs in 4 groups of osteoblasts with varying mineralization processes. Hsa_circ_0008500 (circ8500), which is upregulated in the RNA-seq data, is sifted through 194 candidate circRNAs in osteoblasts during mineralization. We characterize the features of novel circRNAs and find that the elevated expression of circ8500 promotes osteoblast mineralization. Mechanistically, circ8500 contains a critical binding site for miR-1301-3p. We further show that circ8500 competitively binds miR-1301-3p to abolish its suppressive effect on peptidyl arginine deiminase 4 (PADI4). PADI4 works as a binding partner of RUNX2 and stabilizes its protein expression levels by inhibiting the ubiquitin-proteasome pathway. This work provides new insights on the circRNA patterns in osteoblasts and the role of PADI4 in matrix mineralization.

| S-EPMC7759526 | biostudies-literature

Effect of CCAR1 depletion on androgen-dependent gene expression in LNCaP cells

Project description:Androgen receptor (AR) plays a critical role in prostate cancer onset and progression, and cell cycle and apoptosis regulator 1 (CCAR1) functions as an AR co-activator. We performed genome-wide gene expression analysis in control (shNS) and CCAR1-depleted (shCCAR1) LNCaP cells to assess the global effect of CCAR1 on the expression of androgen responsive genes. LNCaP cells expressing shNS or shCCAR1 were treated with ethanol or 10 nM DHT for 24 hr, and total RNA was isolated using the RNeasy mini kit (Qiagen). The integrity of RNA was analyzed using an Agilent 2100 Bioanalyzer. Two independent biological replicates were assayed for each sample. The microarrays were performed following the Affymetrix standard protocol.

2013-10-01 | E-GEOD-45033 | biostudies-arrayexpress

The Splicing Factor CCAR1 Regulates the Fanconi Anemia/BRCA Pathway

Project description:The twenty-three Fanconi Anemia proteins cooperate in a DNA repair pathway, called the FA/BRCA pathway, required for the monoubiquitination of FANCD2 and the excision of interstrand DNA crosslinks (ICLs). The CCAR1 (cell division cycle and apoptosis regulator 1) protein is also a regulator of ICL repair, though its possible function in the FA/BRCA pathway remains unknown. Here, we demonstrate that CCAR1 plays a unique upstream role in the FA/BRCA pathway and is required for FANCA protein expression and FANCD2 monoubiquitination. Interestingly, loss of CCAR1 results in retention of a poison exon in the FANCA transcript, thereby leading to reduced FANCA protein expression. A unique domain of CCAR1, the so-called EF-hand domain, binds to the spliceosome SF3B complex and is required for its mRNA splicing activity. Taken together, CCAR1 is a unique splicing factor, required for normal splicing of the FANCA mRNA and perhaps other mRNAs involved in various cellular pathways.

2024-08-21 | GSE242781 | GEO

Effect of CCAR1 depletion on androgen-dependent gene expression in LNCaP cells

2013-10-01 | GSE45033 | GEO