COX-2 specific inhibitors enhance the cytotoxic effects of pemetrexed in mesothelioma cell lines

O’Kane, Sara L.; Greenman, John; Lind, Michael; Cawkwell, Lynn

doi:10.1016/j.lungcan.2009.04.008

Cited by 29 publications

(21 citation statements)

References 31 publications

(32 reference statements)

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“…Thus, reinforcing the evidence of COX-2 primary role in the pathogenesis and progression of malignant mesothelioma (36,37). Because of the lack of reliable treatment capable of achieving long-term control in patients with mesothelioma, these enzymes are becoming more and more credible as potential therapeutic targets (19,38,39). Celecoxib, a nonsteroidal anti-inflammatory drug (NSAID) and selective COX-2 inhibitor, in association with other drugs, is used in malignant mesothelioma clinical trials (Table 1).…”

Section: Cyclooxygenasesmentioning

confidence: 82%

Cyclooxygenase-2, Epidermal Growth Factor Receptor, and Aromatase Signaling in Inflammation and Mesothelioma

Nuvoli¹,

Galati²

2013

Molecular Cancer Therapeutics

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Malignant mesothelioma or mesothelioma is a rare form of cancer that develops from transformed cells originating in the mesothelium, the protective lining that covers many of the internal organs of the body. It is directly linked to asbestos exposure, which acts as a carcinogen by initiating the carcinogenic process. Because of their shape, asbestos fibers can cross the membrane barriers inside the body and cause inflammatory and fibrotic reactions. Such reactions are believed to be the mechanism by which asbestos fibers may trigger malignant mesothelioma in the pleural membrane around the lungs. Carcinogens are known to modulate the transcription factors, antiapoptotic proteins, proapoptotic proteins, protein kinases, cell-cycle proteins, cell adhesion molecules, COX-2, and growth factor signaling pathways. This article reviews recent studies regarding some malignant mesothelioma molecular targets not only for cancer prevention but also for cancer therapy.

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Section: Cyclooxygenasesmentioning

confidence: 82%

Cyclooxygenase-2, Epidermal Growth Factor Receptor, and Aromatase Signaling in Inflammation and Mesothelioma

Nuvoli¹,

Galati²

2013

Molecular Cancer Therapeutics

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“…COX-2 may promote proliferation, angiogenesis and invasiveness, prevent apoptosis and enhance cell adhesion and motility (42). Treatment with COX-2-specific inhibitors results in a wide range of cellular effects, including induction of apoptosis, reduction of cell proliferation, inhibition of angiogenesis and enhanced anticancer drug-induced cytotoxicity (43)(44)(45)(46). These findings suggest that NSAIDs may exert their anticancer effects through COX-2 inhibition.…”

Section: Coxs and Their Inhibitors In Cancer Treatmentmentioning

confidence: 99%

Potency of non-steroidal anti-inflammatory drugs in chemotherapy

Hiľovská

Jendželovský

Fedoročko

2014

Molecular and Clinical Oncology

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“…This finding enriches our understanding of the tumorigenic pathway that leads to esophageal cancer growth. As mentioned earlier, prostaglandin pathway remains one of the well validated pathway for drug development for chemoprevention, but COX-2 specific inhibitors has formidable cardiovascular effects that has prohibited their widespread use (McKenna et al, 2001;Solomon et al, 2004;Wolfe et al, 2004;Zhao et al, 2004;Schaefer et al, 2005;O'Kane et al, 2010). On the other hand, it will be of enormous clinical benefit if PGDH expression can be induced in premalignant and malignant epithelial cells in esophageal cancer and subsequently suppress tumor growth.…”

Section: Discussionmentioning

confidence: 99%

Expression of PGDH Correlates with Cell Growth in Both Esophageal Squamous Cell Carcinoma and Adenocarcinoma

Yang

Wang²,

Xu³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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Esophageal cancer represents the fourth most common gastrointestinal cancer and generally confers a poor prognosis. Prostaglandin-producing cyclo-oxygenase has been implicated in the pathogenesis of esophageal cancer growth. Here we report that prostaglandin dehydrogenase, the major enzyme responsible for prostaglandin degradation, is significantly reduced in expression in esophageal cancer in comparison to normal esophageal tissue. Reconstitution of PGDH expression in esophageal cancer cells suppresses cancer cell growth, at least in part through preventing cell proliferation and promoting cell apoptosis. The tumor suppressive role of PGDH applies equally to both squamous cell carcinoma and adenocarcinoma, which enriches our understanding of the pathogenesis of esophageal cancer and may provide an important therapeutic target.

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COX-2 specific inhibitors enhance the cytotoxic effects of pemetrexed in mesothelioma cell lines

Cited by 29 publications

References 31 publications

Cyclooxygenase-2, Epidermal Growth Factor Receptor, and Aromatase Signaling in Inflammation and Mesothelioma

Cyclooxygenase-2, Epidermal Growth Factor Receptor, and Aromatase Signaling in Inflammation and Mesothelioma

Potency of non-steroidal anti-inflammatory drugs in chemotherapy

Expression of PGDH Correlates with Cell Growth in Both Esophageal Squamous Cell Carcinoma and Adenocarcinoma

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