Overexpression of lncRNA GAS5 suppresses prostatic epithelial cell proliferation by regulating COX-2 in chronic non-bacterial prostatitis

Xu, Xu; Hou, Jianquan; Lv, Jinxing; Huang, Yuhua; Pu, Jinxian; Wang, Liangliang

doi:10.1080/15384101.2019.1593644

Cited by 23 publications

(19 citation statements)

References 26 publications

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“…In addition, we found that COX-2 was highly expressed in prostate tissues of CP patients. Simultaneously, COX-2 expression was up-regulated in human prostate cells RWPE-1 and CNP rats induced by LPS, which is consistent with previous studies [16,30]. Therefore, elevated COX-2 was a key feature of CNP, which led to an increase in the synthesis of PGE2 and aggravated the inflammatory response in CNP rats.…”

Section: Case Discussionsupporting

confidence: 90%

MiR-181c inhibits prostatic epithelial cell proliferation caused by chronic non-bacterial prostatitis through downregulating COX-2

Huang

Hou

et al. 2020

APT

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Background: Chronic non-bacterial prostatitis (CNP) is a widespread disease of the male reproductive system. MiR-181c can be expressed in prostate tissue, but it has not been reported in CNP. This study aims to investigate the role of miR-181c in CNP and its mechanism of action on CNP, providing new ideas for the treatment and diagnosis of CNP. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting were applied to determine miR-181c expression in clinical CP patients, CNP rats, and LPS-induced human prostaglandin epithelial cell RWPE-1. Then, luciferase reporter assay was performed to verify the targeting relation between miR-181c and COX-2. Through cell transfection experiments, the effect of mi-181c on the expression of COX2 and PGE2 was studied, and the effect of miR-181c/COX-2 on the proliferation of prostate epithelial cells was also explored. Results: qRT-PCR and Western blotting analysis revealed that miR-181c was low expressed in prostate tissue of CP patients and CNP rats and human prostaglandin epithelial cell RWPE-1. The luciferase reporter assay confirmed the targeting relation between miR-181c and COX-2. And miR-181c overexpression reduced the expression of COX-2 and PGE2 and suppressed the proliferation of prostate epithelial cells. COX-2 up-regulation reversed these effects caused by overexpression of miR-181c. Conclusions: miR-181c inhibited the proliferation of prostate epithelial cells through negatively regulating COX-2 to alleviate chronic non-bacterial prostatitis. Keywords: Chronic non-bacterial prostatitis, miR-181c, COX-2, prostatic epithelial cell, proliferation

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Section: Case Discussionsupporting

confidence: 90%

MiR-181c inhibits prostatic epithelial cell proliferation caused by chronic non-bacterial prostatitis through downregulating COX-2

Huang

Hou

et al. 2020

APT

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“…Recent work suggests that the GAS5 lncRNA directly binds to the cyclooxygenase (COX)-2 protein, but the evidence is not convincing [69]. Similarly, another recent publication suggests that GAS5 lncRNA interacts directly with the enzyme glucose-6-phosphate dehydrogenase (G6PD), but the evidence again is weak [70].…”

Section: Gas5 Lncrna As a Scaffold Seeding The Assembly Of A Nuclementioning

confidence: 99%

The Growth-Arrest-Specific (GAS)-5 Long Non-Coding RNA: A Fascinating lncRNA Widely Expressed in Cancers

Goustin

Thepsuwan

Kosir

et al. 2019

ncRNA

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Long non-coding RNA (lncRNA) genes encode non-messenger RNAs that lack open reading frames (ORFs) longer than 300 nucleotides, lack evolutionary conservation in their shorter ORFs, and do not belong to any classical non-coding RNA category. LncRNA genes equal, or exceed in number, protein-coding genes in mammalian genomes. Most mammalian genomes harbor ~20,000 protein-coding genes that give rise to conventional messenger RNA (mRNA) transcripts. These coding genes exhibit sweeping evolutionary conservation in their ORFs. LncRNAs function via different mechanisms, including but not limited to: (1) serving as “enhancer” RNAs regulating nearby coding genes in cis; (2) functioning as scaffolds to create ribonucleoprotein (RNP) complexes; (3) serving as sponges for microRNAs; (4) acting as ribo-mimics of consensus transcription factor binding sites in genomic DNA; (5) hybridizing to other nucleic acids (mRNAs and genomic DNA); and, rarely, (6) as templates encoding small open reading frames (smORFs) that may encode short proteins. Any given lncRNA may have more than one of these functions. This review focuses on one fascinating case—the growth-arrest-specific (GAS)-5 gene, encoding a complicated repertoire of alternatively-spliced lncRNA isoforms. GAS5 is also a host gene of numerous small nucleolar (sno) RNAs, which are processed from its introns. Publications about this lncRNA date back over three decades, covering its role in cell proliferation, cell differentiation, and cancer. The GAS5 story has drawn in contributions from prominent molecular geneticists who attempted to define its tumor suppressor function in mechanistic terms. The evidence suggests that rodent Gas5 and human GAS5 functions may be different, despite the conserved multi-exonic architecture featuring intronic snoRNAs, and positional conservation on syntenic chromosomal regions indicating that the rodent Gas5 gene is the true ortholog of the GAS5 gene in man and other apes. There is no single answer to the molecular mechanism of GAS5 action. Our goal here is to summarize competing, not mutually exclusive, mechanistic explanations of GAS5 function that have compelling experimental support.

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“…The disease course of CNP is long and presents with complex symptoms [9],which seriously affect patients' quality of life and physical and mental health [10][11][12][13][14][15].Further, it is also associated with shame [16]. According to global statistics, the incidence of CNP ranges from 2.2% to 9.7%, with an average prevalence of 8.2% [17].The pathogenesis and pathophysiology of CNP are not very clear, and the treatment is challenging [18].…”

Section: Discussionmentioning

confidence: 99%

Correlation of pain with Substance P and neurokinin-1 receptor in the L5-S2 spinal cord in rats with chronic nonbacterial prostatitis

Hao

Zhang

Bai

et al. 2020

Preprint

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BackgroundTo investigate the correlation of the pain with the expression of SP and NK-1R in the posterior horn of the L5-S2 spinal cord in a rat model of chronic nonbacterial prostatitis (CNP) at different time points of modeling. MethodsForty adult male SD rats were randomly divided into four equal groups: control group, 45 day (d) group, 60 d group, and 90 d group, and proteins were obtained from the prostatic tissue of another 30 rats. The CNP model was established by intraperitoneal injection of 0.5 mL diazepam vaccine and intradermal injection of a mixed solution of 1 mL prostatein extract and complete adjuvant at a 1:1 ratio. The control group rats were injected with the same volume of normal saline. At 45, 60, and 90 days after modeling, we measured the paw withdrawal threshold (PWT) of the rats, detected the level of TNF-α, IL-1ß, IL-2, and IL-10 in the prostate tissues by ELISA, observed the histomorphological changes in the prostate by transmission electron and light microscopy, and detected the expression of SP and NK1-R in the L5-S2 spinal cord by immunohistochemistry. ResultsThe levels of TNF-α, IL-1ß, IL-2, and IL-10 in the prostate tissue were markedly higher in the CNP models than those in the control group(all P<0.05); this difference was Most significant at 90 days (all P<0.05). Immunohistochemistry showed that the expressions of SP and NK-1R were remarkably higher in the CNP model groups than in the control (all P<0.05), with the highest expression found at 90 days. Light microscopy revealed no inflammatory cell infiltration in the prostate tissue of the control rats, and obvious edema and increased lymphocyte count were observed as the duration of modeling increased. Transmission electron microscopy showed inflammatory changes in the prostate tissue of the model rats; peritubular interstitial edema was most obvious at 90 days, with widened gaps between the peritubular cells and epithelial base and increased numbers of fibroblasts and collagen fibrils. ConclusionThere was a correlation between the pain and the expressions of SP and the NK-1R in the L5-S2 spinal cord of the rats.

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Overexpression of lncRNA GAS5 suppresses prostatic epithelial cell proliferation by regulating COX-2 in chronic non-bacterial prostatitis

Cited by 23 publications

References 26 publications

MiR-181c inhibits prostatic epithelial cell proliferation caused by chronic non-bacterial prostatitis through downregulating COX-2

MiR-181c inhibits prostatic epithelial cell proliferation caused by chronic non-bacterial prostatitis through downregulating COX-2

The Growth-Arrest-Specific (GAS)-5 Long Non-Coding RNA: A Fascinating lncRNA Widely Expressed in Cancers

Correlation of pain with Substance P and neurokinin-1 receptor in the L5-S2 spinal cord in rats with chronic nonbacterial prostatitis

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