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http://purl.uniprot.org/citations/37208228http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/37208228http://www.w3.org/2000/01/rdf-schema#comment"

Purpose

To explore the role of circadian clock gene NR1D1 (REV-erbα) in bladder cancer (BC).

Methods

Firstly, the association of NR1D1 level with clinical characteristics and prognosis was investigated among patients diagnosed with BC. Secondly, CCK-8, transwell, and colony formation experiments were performed among BC cells treated with Rev-erbα agonist (SR9009), as well as lentivirus and siRNA, for which NR1D1 were overexpressed (OE) and knocked down (KD), respectively. Thirdly, cell cycle and apoptosis were tested by flowcytometry. PI3K/AKT/mTOR pathway proteins were determined in OE-NR1D1 cells. Finally, OE-NR1D1 and OE-Control BC cells were subcutaneously implanted in BALB/c nude mice. The tumor size and protein levels were compared between groups. A P < 0.05 was considered as statistically significant.

Results

Patients with NR1D1 positive status had a longer disease-free survival than those with negative expression. The cell viability, migration, and colony formation of BC cells after treated with SR9009 were significantly suppressed. OE-NR1D1 cells had obviously inhibited cell viability, migration, and colony formation, while those were found strengthened in KD-NR1D1 cells. Besides, KD-NR1D1 cells were observed with a lower proportion of dead cells and G0/G1 cells, but a higher ratio of G2/M. The changes of p-AKT, p-S6, p-4EBP1, and FASN involved in PI3K/AKT/mTOR pathway were detected in OE- and KD-NR1D1 BC cells. Finally, in vivo data demonstrated that overexpression of NR1D1 suppressed the tumorigenicity of BC cells.

Conclusion

NR1D1 played a role of tumor suppressor and it might become a novel target for the treatment of BC."xsd:string
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http://purl.uniprot.org/citations/37208228http://purl.uniprot.org/core/author"Bai Y."xsd:string
http://purl.uniprot.org/citations/37208228http://purl.uniprot.org/core/author"Feng D."xsd:string
http://purl.uniprot.org/citations/37208228http://purl.uniprot.org/core/author"Guo Y."xsd:string
http://purl.uniprot.org/citations/37208228http://purl.uniprot.org/core/author"Han P."xsd:string
http://purl.uniprot.org/citations/37208228http://purl.uniprot.org/core/author"Li D."xsd:string
http://purl.uniprot.org/citations/37208228http://purl.uniprot.org/core/author"Yu Z."xsd:string
http://purl.uniprot.org/citations/37208228http://purl.uniprot.org/core/author"Zhang F."xsd:string
http://purl.uniprot.org/citations/37208228http://purl.uniprot.org/core/author"Wang X."xsd:string
http://purl.uniprot.org/citations/37208228http://purl.uniprot.org/core/author"Yang Y."xsd:string
http://purl.uniprot.org/citations/37208228http://purl.uniprot.org/core/date"2023"xsd:gYear
http://purl.uniprot.org/citations/37208228http://purl.uniprot.org/core/name"Urol Oncol"xsd:string
http://purl.uniprot.org/citations/37208228http://purl.uniprot.org/core/pages"327.e9-327.e18"xsd:string
http://purl.uniprot.org/citations/37208228http://purl.uniprot.org/core/title"Clock gene NR1D1 might be a novel target for the treatment of bladder cancer."xsd:string
http://purl.uniprot.org/citations/37208228http://purl.uniprot.org/core/volume"41"xsd:string
http://purl.uniprot.org/citations/37208228http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/37208228
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