Tumor protein P63 Regulated 1 contributes to inflammation and cell proliferation of cystitis glandularis through regulating the NF-[kappa]B/cyclooxygenase-2/ prostaglandin E2 axis

Cystitis glandularis is characterized by chronic inflammation and hyperproliferation of the bladder mucosa, and it contributes to the progression of bladder adenocarcinoma. Tumor Protein P63 Regulated 1 (TPRG1) is related to cellular inflammatory response, and dysregulation of TPRG1 in tumor tissues...

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Bibliographic Details
Published in:Bosnian journal of basic medical sciences 2022-02, Vol.22 (1)
Main Authors: Hong, Tao, Piao, Songzhe, Sun, Liangxue, Tao, Yiran, Ke, Mang
Format: Article
Language:English
Subjects:
Bladder cancer
Cell proliferation
Cellular signal transduction
Complications and side effects
COX-2 inhibitors
Cystitis
Development and progression
Genetic aspects
Health aspects
Prostaglandins E
Risk factors
Transcription factors
Tumor proteins
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Summary:Cystitis glandularis is characterized by chronic inflammation and hyperproliferation of the bladder mucosa, and it contributes to the progression of bladder adenocarcinoma. Tumor Protein P63 Regulated 1 (TPRG1) is related to cellular inflammatory response, and dysregulation of TPRG1 in tumor tissues is associated with tumor recurrence. The effect of TPRG1 on cystitis glandularis was investigated in this study. Firstly, bladder specimens were isolated from patients with cystitis glandularis and Escherichia coli-induced cystitis rat. Expression of TPRG1 was found to be up-regulated in the bladder specimen. Moreover, adeno-associated virus (AAV)-mediated silencing of TPRG1 was injected into rat, and data from hematoxylin and eosin (H & E) staining showed that injection with AAV-shTPRG1 ameliorated E. coli-induced histological changes in bladder tissues of rats and suppressed the inflammatory response. Secondly, TPRG1 was also increased in primary cystitis glandularis cells. Knockdown of TPRG1 decreased cell proliferation and suppressed the migration of primary cystitis glandularis cells. Thirdly, cyclooxygenase-2 (COX-2) was up-regulated in the bladder specimens isolated from patients with cystitis glandularis and E. coli-induced cystitis rat. Injection with AAV-shTPRG1 reduced protein expression of COX-2, p65 and prostaglandin E2 (PGE2) in the bladder specimen. Finally, interference of COX-2 attenuated TPRG1 over-expression-induced increase in cell proliferation and migration in the primary cystitis glandularis cells. In conclusion, TPRG1 promoted inflammation and cell proliferation of cystitis glandularis through activation of NF-[kappa]B/ COX2/PGE2 axis. KEYWORDS: Tumor protein P63 regulated 1; inflammation; proliferation; cystitis glandularis; NF-[kappa]B/cyclooxygenase 2/prostaglandin E2
ISSN:1512-8601
DOI:10.17305/bjbms.2021.6763