In vitro and in vivo inhibitory effect of three Cox-2 inhibitors and epithelial-to-mesenchymal transition in human bladder cancer cell lines

Adhim, Zainal; Matsuoka, Takahiro; Bito, Toshinori; Shigemura, Katsumi; Lee, Kyung Mi; Kawabata, Masato; Fujisawa, Masato; Nibu, Ken ichi; Shirakawa, Toshiro

doi:10.1038/bjc.2011.262

Cited by 51 publications

(48 citation statements)

References 33 publications

(42 reference statements)

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“…COX-2 is the rate-limiting enzyme involved in the biosynthesis of prostaglandins and it has been suggested that COX-2 is involved in the development and progression of tumors (39,40). In the present study, knockdown of COX-2 expression by siRNA in MGC-803 cells decreased cell viability and colony formation.…”

Section: Discussionmentioning

confidence: 53%

MicroRNA-144 functions as a tumor suppressor in gastric cancer by targeting cyclooxygenase-2

Yao

Wang

et al. 2018

Exp Ther Med

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Abstract. Gastric cancer (GC) poses a serious public health threat and the 5-year survival rate of patients with GC is low. MicroRNAs (miRNAs/miRs) may serve oncogenic or tumor suppressor functions during tumorigenesis by regulating cell proliferation, apoptosis, migration and invasion and it has been demonstrated that they may be dysregulated in various types of cancer. The present study demonstrated that miR-144 and GATA4 were downregulated in GC tissues and cell lines and suggested that this may be due to hypermethylation. Additionally, miR-144 and GATA4 had synergistic effects on GC cells by repressing cell proliferation and inducing cell cycle arrest and apoptosis. The results of bioinformatics and a luciferase reporter assay indicated that cyclooxygenase-2 (COX-2) is a direct target of miR-144 and that miR-144 negatively regulated the expression of COX-2, which inhibits the viability of GC cells. GATA4 also induced a similar effect on COX-2. Taken together, the results of the present study may improve understanding of the underlying mechanism of miR-144 and GATA4 in GC.

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Section: Discussionmentioning

confidence: 53%

MicroRNA-144 functions as a tumor suppressor in gastric cancer by targeting cyclooxygenase-2

Yao

Wang

et al. 2018

Exp Ther Med

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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]. Treatment of the colorectal cancer cell line HT29 with the novel COX-2 inhibitor Apricoxib has shown promise at least in vitro, reversing EMT [106].…”

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

confidence: 71%

“…In bladder and breast cancer the E-cadherin gene is induced by COX-2 appears to be Snail1 [96,105], in non-small cell lung cancer COX-2 induced Snail1 and Zeb1 [108], whereas in head and neck squamous cancer COX-2 induced Snail1, SIP1/Zeb2 as well as Twist1 [101].…”

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

confidence: 99%

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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“…These findings may suggest that the high-risk Tis pathology trends towards higher sensitivity to celecoxib. Response to celecoxib of high and low grade bladder cancer cell lines have been minimally studied, but the available information suggests that the mechanistic response to celecoxib may differ according to grade of bladder cell lines (42, 43), with potential differential sensitivity. Gee et al,found that celecoxib-induced apoptosis and G0/G1 cell cycle arrest occurred primarily through altered cyclin B1/D1 expression in the low grade cell line (RT-2), whereas it was through Rb up-regulation in the high-grade cell line (UM-UC-3).…”

Section: Discussionmentioning

confidence: 99%

A Randomized Controlled Trial of Celecoxib to Prevent Recurrence of Nonmuscle-Invasive Bladder Cancer

Sabichi

Lee

Grossman

et al. 2011

Cancer Prevention Research

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Significant morbidity and expense result from frequent recurrences of non-muscle invasive bladder cancer (NMIBC) after standard treatment, and carcinoma in situ (Tis) is a poor prognostic factor. Predicated on observational and preclinical data strongly supporting cyclooxygenase-2 (COX-2) in the pathogenesis, and the activity of COX-2 inhibitors, in bladder cancer, we conducted a randomized, double-blind, placebo-controlled trial to determine if celecoxib could reduce the time-to-recurrence (TTR) in NMIBC patients at high risk for recurrence. 146 patients were randomized to celecoxib (200 mg) or placebo orally twice daily for at least 12 months. The average treatment duration was 1.25 years. Primary intent-to-treat analysis revealed celecoxib did not statistically significantly prolong TTR compared with placebo (P = 0.17, log-rank). With a median follow-up of 2.49 years the relative risk of recurrence in the celecoxib vs placebo arms was 0.64 (95% CI, 0.38, 1.17). The recurrence-free rate at 12 months with celecoxib was 88% (95% CI, 0.81,0.96) versus 78% (95% CI, 0.69, 0.89) with placebo. After controlling for covariates with Cox regression analysis, recurrence rates did not differ between the two study arms (HR = 0.69; 95% CI, 0.37,1.29). Celecoxib had a marginally significant effect on reducing metachronous recurrences (vs. placebo) with hazard ratio of 0.56 (95% CI, 0.3,1.06; P=0.075). Celecoxib was well tolerated, with similar adverse events and quality-of-life in both arms. Our clinical trial results do not show a clinical benefit for celecoxib in preventing NMIBC recurrence but further investigation of COX-2 inhibitors in this setting is warranted.

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In vitro and in vivo inhibitory effect of three Cox-2 inhibitors and epithelial-to-mesenchymal transition in human bladder cancer cell lines

Cited by 51 publications

References 33 publications

MicroRNA-144 functions as a tumor suppressor in gastric cancer by targeting cyclooxygenase-2

MicroRNA-144 functions as a tumor suppressor in gastric cancer by targeting cyclooxygenase-2

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

A Randomized Controlled Trial of Celecoxib to Prevent Recurrence of Nonmuscle-Invasive Bladder Cancer

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