Cyclooxygenase-1 and 2 in normal and malignant human ovarian epithelium

Li, Shuanfang; Miner, Kelly; Fannin, Rick D.; Barrett, J. Carl; Davis, Barbara J.

doi:10.1016/j.ygyno.2003.10.053

Cited by 65 publications

(57 citation statements)

References 13 publications

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“…2A, COX-1 is localized to the granulosa cell layers, and confined to the OSE and cortical stroma adjacent to the follicle. In contrast to other cancers in which COX-2 is highly expressed, in ovarian cancer, COX-1 expression is markedly increased (Fig, 2B), as has been shown previously in the hen, human and in rodent models of ovarian cancer [8,23,24]. COX-1 has also been shown to be increased in feline oral squamous cell carcinomas, the only non-gynecological carcinoma reported to have increased COX-1 instead of COX-2 [42].…”

Section: Localization and Quantification Of Cox-1 And Cox-2 In The Hesupporting

confidence: 74%

“…COX enzymes are required for ovarian function and many female reproductive processes, but overexpression of COX is associated with significant pathology. Increased expression of COX-2 is associated with manyepithelial carcinomas; however, COX-1 but not COX-2 overexpression has been shown to be associated with ovarian cancer [8,[21][22][23][24][25][26]. The laying hen provides an excellent model for studying normal ovarian functions, in particular ovulation [27,28].…”

Section: Discussionmentioning

confidence: 99%

“…In contrast to most malignancies, however, COX-2 expression is downregulated in ovarian cancer [20]. Instead, COX-1 expression has been shown to be elevated in ovarian cancer [8,[21][22][23][24][25][26]. Whereas considerable research has focused on the role of COX-2 in ovulation and normal ovarian function, much less is known about COX-1.…”

Section: Introductionmentioning

confidence: 99%

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Cyclooxygenases expression and distribution in the normal ovary and their role in ovarian cancer in the domestic hen (Gallus domesticus)

Hales

Zhuge

Lagman

et al. 2008

Endocr

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Cyclooxygenase (COX) (PTGS) is the rate-limiting enzyme in the biosynthesis of prostaglandins. Two COX isoforms have been identified, COX-1 and COX-2, which show distinct cell-specific expression and regulation. Ovarian cancer is the most lethal gynecological malignancy and the © Humana Press Inc. 2008 Correspondence to: Dale Buchanan Hales, dbhale@uic.edu. HHS Public Access Author ManuscriptAuthor Manuscript Author ManuscriptAuthor Manuscript disease is poorly understood due to the lack of suitable animal models. The laying hen spontaneously develops epithelial ovarian cancer with few or no symptoms until the cancer has progresses to a late stage, similar to the human disease. The purpose of this study was to examine the relative expression and distribution of COX-1 and COX-2 in the ovaries of normal hens and in hens with ovarian cancer. The results demonstrate that COX-1 was localized to the granulosa cell layer and cortical interstitium, ovarian surface epithelium (OSE) and postovulatory follicle (POF) of the normal ovary. In ovarian cancer, COX-1 mRNA was significantly increased and COX-1 protein was broadly distributed throughout the tumor stroma. COX-2 protein was localized to the granulosa cell layer in the follicle and the ovarian stroma. COX-2 mRNA expression did not change as a function of age or in ovarian cancer. There was significantly higher expression of COX-1 mRNA in the first POF (POF-1) compared to POF-2 and POF-3. COX-2 mRNA expression was not significantly different among POFs. There was no difference in COX-1 or COX-2 mRNA in the OSE isolated from individual follicles in the follicular hierarchy. The results confirm previous findings of the high expression of COX-1 in ovarian tumors further supporting the laying hen as a model for ovarian cancer, and demonstrate for the first time the high expression of COX-1 in POF-1 which is the source of prostaglandins needed for oviposition.

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Section: Localization and Quantification Of Cox-1 And Cox-2 In The Hesupporting

confidence: 74%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Cyclooxygenases expression and distribution in the normal ovary and their role in ovarian cancer in the domestic hen (Gallus domesticus)

Hales

Zhuge

Lagman

et al. 2008

Endocr

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“…Mechanistic study suggested that expression of COX-2 in uterine cervical carcinoma cells downregulated apoptotic processes and thus enhanced tumour invasion and metastasis (Affney et al, 2001). Li et al (2004) described that while COX-2 protein was not detected in normal epithelium of the ovary, its protein was frequently expressed in ovarian epithelial carcinoma, suggesting that it might contribute to the carcinoma development or progression. Matsumoto et al (2001) found a significant correlation between expression of vascular endothelial growth factor (VEGF) and COX-2 in ovarian neoplasms and suggested that an increased expression of COX-2 might be associated with malignant transformation and tumorigenesis through the activation of VEGF.…”

Section: Discussionmentioning

confidence: 99%

Clinical implication of expression of cyclooxygenase-2 and peroxisome proliferator activated-receptor γ in epithelial ovarian tumours

et al. 2004

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Expression of cyclooxygenase (COX)-2 plays a key role in tumorigenesis and development and peroxisome proliferator-activated receptor g (PPARg) has been implicated in the control of COX-2 expression in some tissues. The aim of this study is to investigate (1) whether expression of COX-2 and PPARg is associated with ovarian carcinogenesis and progression of ovarian tumours and (2) whether COX-2 expression is controlled through ligand-mediated activation of PPARg in ovarian carcinoma cells. For this purpose, the presence of COX-2 and PPARg was immunohistochemically examined in 71 epithelial ovarian carcinomas, 18 borderline tumours and 23 benign tumours and the levels of COX-2 and PPARg proteins were determined by enzyme immunoassay in four benign tumours, three borderline tumours and 12 carcinomas. The frequency of COX-2 and PPARg detection was significantly increased and decreased as lesions progressed to carcinoma, respectively. The COX-2 protein was not detected in the three borderline tumours, whereas PPARg protein was detected in all of them. COX-2 protein was detected in eight of the 12 carcinomas, whereas PPARg protein was detected in only two cases. In addition, PPARg protein was not detected in all of the eight carcinomas in which COX-2 protein was detected, suggesting that expression of PPARg and COX-2 was in a reciprocal relationship. Furthermore, in cultured ovarian carcinoma cells, Western blot revealed that PPARg and COX-2 expression was regulated conversely as a result of stimulation by 15-deoxy-D 12, 14 PGJ 2 (15-PGJ 2 ), a PPARg activator. In addition, 15d-PGJ 2 suppressed tumour necrosis factor-ainduced-COX-2 expression, confirming the reciprocal correlation between COX-2 and PPARg. From these results, it was suggested that PPARg activation might suppress COX-2 expression via the nuclear factor-kB pathway in the ovarian carcinoma cells and that low expression of PPARg and high expression of COX-2 might be involved in carcinogenesis and progression of ovarian tumours.

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“…Several recent studies have shown that COX-2 is overexpressed in epithelial ovarian and primary peritoneal cancers and that overexpression correlates with worse clinical behavior. [25][26][27][28][29] COX-2 overexpression was noted in 65% to 75% of serous ovarian carcinomas studied. It was associated with increased tumor vascularity.…”

Section: Recently Kurman Et Al Proposed a New Classification Ofmentioning

confidence: 94%

Molecular typing of epithelial ovarian carcinomas using inflammatory markers

Ali-Fehmi

Semaan

Sethi

et al. 2010

Cancer

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BACKGROUND: Ovarian epithelial carcinomas have recently been classified as slow growing type I tumors and rapidly growing highly aggressive type II tumors. The present study sought to molecularly characterize type I and II tumors using known molecular markers. METHODS: Specimens from 213 patients with ovarian carcinoma were categorized as type I or type II, and evaluated by immunohistochemistry for the inflammatory markers glucose transporter protein-1 (Glut-1), inducible nitric oxide synthase (iNOS), cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), and nuclear factor kappa B. Statistical analysis was performed to investigate whether these molecular markers could distinguish between type I and type II tumors. Kaplan-Meier survival curves and COX regression analysis were used to determine the prognostic effect of these markers on survival in the 2 types of tumors. RESULTS: Overexpression of COX-1, COX-2, iNOS, and Glut-1 was significantly higher in type II tumors (P < .05). Women with type II tumors had a poorer median survival (60 months) as compared with those with type I tumors (141 months) (P ¼.0001). Multivariate analysis revealed type II tumors, late stage, and age >60 years as significant predictors of poor survival. For type II tumors, median survival of patients with tumors overexpressing COX-2 was 44 compared with 85 months for those with tumors with low COX-2 expression (P ¼.029). Looking at both type I and II tumors, the number of markers simultaneously overexpressed in each tumor was a significant predictor of poor patient survival (P ¼.005). CONCLUSIONS: The present study demonstrates that the new proposed histologic classification of ovarian epithelial carcinomas correlates with a distinct expression of inflammatory pathway proteins. High expression of these markers may explain the different biologic behavior of these 2 tumor types and provide targets for therapy. Cancer 2011;117:301-9.

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Cyclooxygenase-1 and 2 in normal and malignant human ovarian epithelium

Cited by 65 publications

References 13 publications

Cyclooxygenases expression and distribution in the normal ovary and their role in ovarian cancer in the domestic hen (Gallus domesticus)

Cyclooxygenases expression and distribution in the normal ovary and their role in ovarian cancer in the domestic hen (Gallus domesticus)

Clinical implication of expression of cyclooxygenase-2 and peroxisome proliferator activated-receptor γ in epithelial ovarian tumours

Molecular typing of epithelial ovarian carcinomas using inflammatory markers

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