Reciprocal correlation between the expression of cyclooxygenase-2 and E-cadherin in human bladder transitional cell carcinomas

Jang, Tae Jung; Heon, Woo; Lee, Kyung Seob

doi:10.1007/s00428-010-0943-3

Cited by 22 publications

(24 citation statements)

References 32 publications

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“…Similar results were obtained by Jang et al (2010), who found that the expression of E-cadherin decreases in case of HG tumors.…”

Section: Disscussionsupporting

confidence: 89%

Immunohistochemical Analysis of Urothelial Bladder Cancers

Bevizova¹

2013

OnLine Journal of Biological Sciences

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Malignant cancers of urinary bladder are the second most common malignancy of the urinary tract and the fourth most common malignancy in general, especially in men. The aim of this study was a retrospective analysis of selected markers (p53, Ki-67 and E-cadherin) of urinary bladder cancers from the Department of Urology in Bratislava, Slovak Republic between years 2007 and 2009. We analysed 244 patients (202 males, 42 females) with diagnosed bladder cancer via cystoscopy and subsequent transurethral resection. Patients' age varied from 36 to 98 years. Obtained samples were fixed by 10% buffered formalin for 24 to 48 h. Subsequently, they were dehydrated in ascending ethanol series and embedded in paraffin. The parafin sections of 5 µ m were prepared by microtome and they were stained by haematoxylin and eosin. The antibodies against to p53, Ki-67 and E-cadherin were used in immunohistochemical analysis. Statistical evaluation was performed via SPSS using non-parametric Kruskal-Wallis test and p values<0.05 were considered statistically significant. No significant differences in the expression of selected markers were found between genders. Expression of p53 and Ki-67, in G1 and G2 of low grade tumours was lower in comparison to their expression in G3 tumors. Expression of E-cadherin was the opposite in this case. The expression of p53 and Ki-67 positively correlated with tumor's depth of invasion, while the expression of E-cadherin significantly decreased. In case of T4 tumors, the expression of all markers exhibited consistently high values. When analysing tumor multiplicity, the expression of p53 and Ki-67 significantly decreased, while the expression of E-cadherin significantly increased. Based on the obtained results it can be concluded that the analysis of p53, Ki-67 and E-cadherin expression is essential for diagnostics and prognostics of bladder cancer and should be routinely used in daily practise together with "conventional" markers to improve prognosis estimation.

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“…Similar results were obtained by Jang et al (2010), who found that the expression of E-cadherin decreases in case of HG tumors.…”

Section: Disscussionsupporting

confidence: 89%

Immunohistochemical Analysis of Urothelial Bladder Cancers

Bevizova¹

2013

OnLine Journal of Biological Sciences

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“…Thus, Celecoxib was found to be effective in upregulating E-cadherin thus reversing the EMT in cell lines derived from head and neck squamous cancer, colon cancer, gastric cancer and breast cancer [101][102][103][104]. Another COX-2 inhibitor, Etodolac, had a similar effect in bladder cancer cell lines, where EMT reversal was also seen in vivo in xenografts of the human bladder cancer cell line T24 [105].…”

Section: Cox-2 Is Associated With Breast Cancer Invasion Via Emtmentioning

confidence: 67%

New Insights on COX-2 in Chronic Inflammation Driving Breast Cancer Growth and Metastasis

Hugo

Saunders

Ramsay

et al. 2015

J Mammary Gland Biol Neoplasia

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The medicinal use of aspirin stretches back to ancient times, before it was manufactured in its pure form in the late 19th century. Its accepted mechanistic target, cyclooxygenase (COX), was discovered in the 1970s and since this landmark discovery, the therapeutic application of aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) has increased dramatically. The most significant benefits of NSAIDs are in conditions involving chronic inflammation (CI). Given the recognized role of CI in cancer development, the use of long-term NSAID treatment in the prevention of cancer is an enticing possibility. COX-2 is a key driver of CI, and here we review COX-2 expression as a predictor of survival in various cancer types, including breast. Obesity and post-partum involution are natural inflammatory states that are associated with increased breast cancer risk. We outline the COX-2 mediated mechanisms contributing to the growth of cancers. We dissect the cellular mechanism of epithelial-mesenchymal transition (EMT) and how COX-2 may induce this to facilitate tumor progression. Finally we examine the potential regulation of COX-2 by c-Myb, and the possible interplay between c-Myb/COX-2 in proliferation, and hypoxia inducible factor-1 alpha (HIF1α)/COX-2 in invasive pathways in breast cancer.

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“…COX-2 expression was significantly higher in SCC than in precursors and NS (p < 0.05). An inverse correlation was found between the expression of COX-2 and E-cadherin in a variety of tumors [18,29]. We found COX-2 expression in 68 % (13 out of 19) of SCC with focal loss of E-cadherin and in 22 % (6 out of 22) of SCC with normal expression of E-cadherin (p00.008).…”

Section: Resultsmentioning

confidence: 61%

“…Induction of PGE 2 represses E-cadherin expression through the induction of Snail and ZEB1 in non-small cell lung cancer and colon cancer [18,33,34]. Ectopic expression of COX-2 in or PGE 2 treatment of bladder cancer cells reduces E-cadherin expression [29]. Recently it was found that E-cadherin expression is inhibited via the PGE 2 -EP2 signaling pathway during ultraviolet-induced cutaneous squamous cell carcinoma progression [17].…”

Section: Discussionmentioning

confidence: 97%

Epithelial to mesenchymal transition in cutaneous squamous cell carcinoma is correlated with COX-2 expression but not with the presence of stromal macrophages or CD10-expressing cells

Jang

2012

Virchows Arch

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Epithelial to mesenchymal transition (EMT) is an intricate process by which epithelial cells loose epithelial characteristics and acquire a mesenchymal-like phenotype. EMT and cyclooxygenase 2 (COX-2) expression are related to tumor invasion and metastasis. The tumor microenvironment plays a major role in tumor progression and the induction of EMT. Here, we investigated the relationship between EMT and COX-2 expression as well as tumor-associated macrophages (TAM) and CD10-positive stromal cells during the development of cutaneous squamous neoplastic lesion. We performed immunohistochemical staining for vimentin, E-cadherin, β-catenin, COX-2, CD68, and CD10 in 41 cases of squamous cell cancers (SCC), 20 of Bowen's disease, 30 of actinic keratosis, and 30 samples of normal skin. SCC cells showed significantly increased vimentin expression and reduced expression of membranous E-cadherin and β-catenin compared with cells in precursor lesions and in normal skin. COX-2 expression was also markedly increased in SCC cells. E-cadherin expression was positively correlated with β-catenin expression and inversely correlated with COX-2 expression in SCC cells. The number of TAM and CD10-positive stromal cells increased from the normal skin to precursor lesions and SCC cells. The number of TAM and of CD10-positive stromal cells did not correlate with the expression of E-cadherin, β-catenin, COX-2, and vimentin in SCC cells. We suggest that cutaneous SCC cells show EMT, which appears to be correlated with COX-2 expression but not with stromal CD10 expression and TAM.

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Reciprocal correlation between the expression of cyclooxygenase-2 and E-cadherin in human bladder transitional cell carcinomas

Cited by 22 publications

References 32 publications

Immunohistochemical Analysis of Urothelial Bladder Cancers

Immunohistochemical Analysis of Urothelial Bladder Cancers

New Insights on COX-2 in Chronic Inflammation Driving Breast Cancer Growth and Metastasis

Epithelial to mesenchymal transition in cutaneous squamous cell carcinoma is correlated with COX-2 expression but not with the presence of stromal macrophages or CD10-expressing cells

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