Matches in SemOpenAlex for { <https://semopenalex.org/work/W2343575524> ?p ?o ?g. }
- W2343575524 endingPage "128" @default.
- W2343575524 startingPage "116" @default.
- W2343575524 abstract "Limited information is available on the pathologic significance of human antigen R (HuR) in prostate cancer (PCa). The main aim of this study was to clarify the relationship between HuR expression and malignant aggressiveness, outcome, and expression of cancer-related molecules in PCa. In vitro proliferation, colony formation, and migration assays were performed on LNCaP and PC-3 cells. HuR expression was knocked down (KD) using small interfering RNA. The relationships between HuR expression and the expression of vascular endothelial growth factors (VEGFs), cyclooxygenase (COX)-2, and heme oxygenase (HO)-1 were investigated in PCa cell lines using Western blotting. On KD of HuR, cell proliferation and migration were suppressed in both LNCaP and PC-3 cells, whereas expression of VEGF-A to -D and COX-2 was suppressed in PC-3 but not in LNCaP cells. In addition, expression of these cancer-related factors was analyzed in 182 hormone-naïve PCa and 23 castration-resistant prostate cancer (CRPC) human tissues in vivo. Cytoplasmic (C)-HuR expression was significantly higher in CRPC > hormone-naïve PCa > nontumoral cells. C-HuR expression was positively associated with Gleason score, T stage, and metastasis, and it was considered to be a useful predictor of biochemical recurrence after radical prostatectomy. C-HuR expression was correlated with COX-2 expression in hormone-naïve PCa, and with the expression of VEGF-A, VEGF-C, and COX-2 in CRPC tissues. Our results demonstrated that HuR plays important roles in determining malignant aggressiveness and outcome in PCa, especially in androgen-independent PCa cells, via the regulation of cell proliferation, migration, and expression of VEGF-A, -C, and COX-2. Limited information is available on the pathologic significance of human antigen R (HuR) in prostate cancer (PCa). The main aim of this study was to clarify the relationship between HuR expression and malignant aggressiveness, outcome, and expression of cancer-related molecules in PCa. In vitro proliferation, colony formation, and migration assays were performed on LNCaP and PC-3 cells. HuR expression was knocked down (KD) using small interfering RNA. The relationships between HuR expression and the expression of vascular endothelial growth factors (VEGFs), cyclooxygenase (COX)-2, and heme oxygenase (HO)-1 were investigated in PCa cell lines using Western blotting. On KD of HuR, cell proliferation and migration were suppressed in both LNCaP and PC-3 cells, whereas expression of VEGF-A to -D and COX-2 was suppressed in PC-3 but not in LNCaP cells. In addition, expression of these cancer-related factors was analyzed in 182 hormone-naïve PCa and 23 castration-resistant prostate cancer (CRPC) human tissues in vivo. Cytoplasmic (C)-HuR expression was significantly higher in CRPC > hormone-naïve PCa > nontumoral cells. C-HuR expression was positively associated with Gleason score, T stage, and metastasis, and it was considered to be a useful predictor of biochemical recurrence after radical prostatectomy. C-HuR expression was correlated with COX-2 expression in hormone-naïve PCa, and with the expression of VEGF-A, VEGF-C, and COX-2 in CRPC tissues. Our results demonstrated that HuR plays important roles in determining malignant aggressiveness and outcome in PCa, especially in androgen-independent PCa cells, via the regulation of cell proliferation, migration, and expression of VEGF-A, -C, and COX-2. Mitsunari K, et al.At a Glance CommentaryBackgroundProstate cancer is one of the most common cancer worldwide, and prognosis of castration-resistant prostate cancer (CRPC) is poor despite various treatments are performed. Relationships between human antigen R (HuR) and clinicopathologic features, prognosis, and malignant potential including cancer cell proliferation, migration, vascular endothelial growth factors (VEGFs), cyclooxygenase (COX)-2, and heme oxygenase (HO)-1 in prostate cancer are not clear.Translational SignificanceHuR played important roles for tumor growth, progression, and biochemical recurrence via regulation of cell proliferation, migration, and COX-2 expression in androgen-naïve cancer cells. In addition to these variables, HuR expression was associated with VEGF-A and -C in androgen-independent cells and CRPC. Prostate cancer is one of the most common cancer worldwide, and prognosis of castration-resistant prostate cancer (CRPC) is poor despite various treatments are performed. Relationships between human antigen R (HuR) and clinicopathologic features, prognosis, and malignant potential including cancer cell proliferation, migration, vascular endothelial growth factors (VEGFs), cyclooxygenase (COX)-2, and heme oxygenase (HO)-1 in prostate cancer are not clear. HuR played important roles for tumor growth, progression, and biochemical recurrence via regulation of cell proliferation, migration, and COX-2 expression in androgen-naïve cancer cells. In addition to these variables, HuR expression was associated with VEGF-A and -C in androgen-independent cells and CRPC." @default.
- W2343575524 created "2016-06-24" @default.
- W2343575524 creator A5027874681 @default.
- W2343575524 creator A5050794980 @default.
- W2343575524 creator A5051928225 @default.
- W2343575524 creator A5075087907 @default.
- W2343575524 creator A5077488645 @default.
- W2343575524 creator A5079627883 @default.
- W2343575524 creator A5084815637 @default.
- W2343575524 date "2016-09-01" @default.
- W2343575524 modified "2023-10-18" @default.
- W2343575524 title "Human antigen R is positively associated with malignant aggressiveness via upregulation of cell proliferation, migration, and vascular endothelial growth factors and cyclooxygenase-2 in prostate cancer" @default.
- W2343575524 cites W1253031956 @default.
- W2343575524 cites W1969920728 @default.
- W2343575524 cites W1972671221 @default.
- W2343575524 cites W1980227325 @default.
- W2343575524 cites W1981781176 @default.
- W2343575524 cites W1982925662 @default.
- W2343575524 cites W1992662084 @default.
- W2343575524 cites W1993691900 @default.
- W2343575524 cites W1993841930 @default.
- W2343575524 cites W2001724396 @default.
- W2343575524 cites W2014994440 @default.
- W2343575524 cites W2032124985 @default.
- W2343575524 cites W2033300742 @default.
- W2343575524 cites W2033695475 @default.
- W2343575524 cites W2043847498 @default.
- W2343575524 cites W2050489269 @default.
- W2343575524 cites W2057941286 @default.
- W2343575524 cites W2064492560 @default.
- W2343575524 cites W2067437913 @default.
- W2343575524 cites W2067908058 @default.
- W2343575524 cites W2076495416 @default.
- W2343575524 cites W2082447227 @default.
- W2343575524 cites W2105293913 @default.
- W2343575524 cites W2125043493 @default.
- W2343575524 cites W2127243900 @default.
- W2343575524 cites W2133150504 @default.
- W2343575524 cites W2140855177 @default.
- W2343575524 cites W2146561872 @default.
- W2343575524 cites W2148221199 @default.
- W2343575524 cites W2155416916 @default.
- W2343575524 cites W2158503538 @default.
- W2343575524 cites W2161536885 @default.
- W2343575524 cites W2162669436 @default.
- W2343575524 cites W2163085311 @default.
- W2343575524 cites W2168377000 @default.
- W2343575524 cites W2168930852 @default.
- W2343575524 cites W2235560983 @default.
- W2343575524 doi "https://doi.org/10.1016/j.trsl.2016.04.002" @default.
- W2343575524 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27140699" @default.
- W2343575524 hasPublicationYear "2016" @default.
- W2343575524 type Work @default.
- W2343575524 sameAs 2343575524 @default.
- W2343575524 citedByCount "30" @default.
- W2343575524 countsByYear W23435755242016 @default.
- W2343575524 countsByYear W23435755242017 @default.
- W2343575524 countsByYear W23435755242018 @default.
- W2343575524 countsByYear W23435755242019 @default.
- W2343575524 countsByYear W23435755242020 @default.
- W2343575524 countsByYear W23435755242021 @default.
- W2343575524 countsByYear W23435755242022 @default.
- W2343575524 countsByYear W23435755242023 @default.
- W2343575524 crossrefType "journal-article" @default.
- W2343575524 hasAuthorship W2343575524A5027874681 @default.
- W2343575524 hasAuthorship W2343575524A5050794980 @default.
- W2343575524 hasAuthorship W2343575524A5051928225 @default.
- W2343575524 hasAuthorship W2343575524A5075087907 @default.
- W2343575524 hasAuthorship W2343575524A5077488645 @default.
- W2343575524 hasAuthorship W2343575524A5079627883 @default.
- W2343575524 hasAuthorship W2343575524A5084815637 @default.
- W2343575524 hasBestOaLocation W23435755241 @default.
- W2343575524 hasConcept C121608353 @default.
- W2343575524 hasConcept C126322002 @default.
- W2343575524 hasConcept C167734588 @default.
- W2343575524 hasConcept C2777025900 @default.
- W2343575524 hasConcept C2779723316 @default.
- W2343575524 hasConcept C2780192828 @default.
- W2343575524 hasConcept C502942594 @default.
- W2343575524 hasConcept C54355233 @default.
- W2343575524 hasConcept C62112901 @default.
- W2343575524 hasConcept C71924100 @default.
- W2343575524 hasConcept C86803240 @default.
- W2343575524 hasConceptScore W2343575524C121608353 @default.
- W2343575524 hasConceptScore W2343575524C126322002 @default.
- W2343575524 hasConceptScore W2343575524C167734588 @default.
- W2343575524 hasConceptScore W2343575524C2777025900 @default.
- W2343575524 hasConceptScore W2343575524C2779723316 @default.
- W2343575524 hasConceptScore W2343575524C2780192828 @default.
- W2343575524 hasConceptScore W2343575524C502942594 @default.
- W2343575524 hasConceptScore W2343575524C54355233 @default.
- W2343575524 hasConceptScore W2343575524C62112901 @default.
- W2343575524 hasConceptScore W2343575524C71924100 @default.
- W2343575524 hasConceptScore W2343575524C86803240 @default.
- W2343575524 hasFunder F4320334764 @default.
- W2343575524 hasLocation W23435755241 @default.
- W2343575524 hasLocation W23435755242 @default.
- W2343575524 hasOpenAccess W2343575524 @default.