Perioperative cyclooxygenase 2 inhibition to reduce tumor cell adhesion and metastatic potential of circulating tumor cells in non–small cell lung cancer

Backhus, Leah M.; Sievers, Eric M.; Lin, Gloria Y.; Castanos, Roberto; Bart, Robert D.; Starnes, Vaughn A.; Bremner, Ross M.

doi:10.1016/j.jtcvs.2005.10.060

Cited by 23 publications

(20 citation statements)

References 34 publications

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“…PGE 2 enhances the metastatic process via multiple mechanisms that in combination yield a strong pro-metastatic effect. The effects of PGE 2 that promote metastasis include upregulation of the cell adhesion receptor, CD44 (56, 58, 59), induction of a transition from an epithelial to a mesenchymal phenotype (16, 20, 60), activation of matrix metalloproteinases (23, 54, 61), enhanced tumor cell migration (62), increased angiogenesis (63), and disruption of the immune surveillance of tumor cells (24, 26, 64–66). …”

Section: Discussionmentioning

confidence: 99%

Inhibition of the Biosynthesis of Prostaglandin E2 By Low-Dose Aspirin: Implications for Adenocarcinoma Metastasis

Boutaud

Sosa

Amin

et al. 2016

Cancer Prevention Research

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Meta-analyses have demonstrated that low dose aspirin reduces the risk of developing adenocarcinoma metastasis, and when colon cancer is detected during aspirin treatment, there is a remarkable 83% reduction in risk of metastasis. As platelets participate in the metastatic process, the anti-platelet action of low dose aspirin likely contributes to its anti-metastatic effect. Cycloxooxygenase-2 (COX-2)-derived prostaglandin E2 (PGE2) also contributes to metastasis, and we addressed the hypothesis that low dose aspirin also inhibits PGE2 biosynthesis. We show that low dose aspirin inhibits systemic PGE2 biosynthesis by 45% in healthy volunteers (p <0.0001). Aspirin is found to be more potent in colon adenocarcinoma cells than in the platelet, and in lung adenocarcinoma cells its inhibition is equivalent to that in the platelet. Inhibition of COX by aspirin in colon cancer cells is in the context of the metastasis of colon cancer primarily to the liver, the organ exposed to the same high concentrations of aspirin as the platelet. We find that the interaction of activated platelets with lung adenocarcinoma cells up-regulates COX-2 expression and PGE2 biosynthesis, and inhibition of platelet COX-1 by aspirin inhibits PGE2 production by the platelet-tumor cell aggregates. In conclusion, low dose aspirin has a significant effect on extraplatelet cyclooxygenase, and potently inhibits COX-2 in lung and colon adenocarcinoma cells. This supports a hypothesis that the remarkable prevention of metastasis from adenocarcinomas, and particularly from colon adenocarcinomas, by low dose aspirin results from its effect on platelet COX-1 combined with inhibition of PGE2 biosynthesis in metastasizing tumor cells.

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Section: Discussionmentioning

confidence: 99%

Inhibition of the Biosynthesis of Prostaglandin E2 By Low-Dose Aspirin: Implications for Adenocarcinoma Metastasis

Boutaud

Sosa

Amin

et al. 2016

Cancer Prevention Research

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“…One study demonstrated that celecoxib suppresses cancer progression, in addition to its analgesic and anti-inflammatory effect (20). Furthermore, it has been shown that perioperative COX-2 inhibition reduces the adhesion and metastatic potential of disseminating tumors in murine models and improves cancer recurrence-free survival rates in mice undergoing primary tumor excision (21). Celecoxib may exert its antitumor effect via COX-2-dependent and -independent pathways.…”

Section: Discussionmentioning

confidence: 99%

Celecoxib inhibits insulin-like growth factor 1 induced growth and invasion in non-small cell lung cancer

Liu

Bao

et al. 2013

Oncology Letters

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Despite a large number of studies indicating that celecoxib plays an important role in the prevention and treatment of tumors, the detailed molecular mechanisms are not well understood. The aim of the present study was to investigate the effect of celecoxib on insulin-like growth factor 1 (IGF-1)-induced growth and invasion in non-small cell lung cancer (NSCLC). For these experiments, IGF-1-induced cell growth and invasion were analyzed in A549 cells in the presence and absence of celecoxib. The effects of celecoxib on the expression of phosphorylated type-1 IGF receptor (IGF-1R) and phosphorylated AKT (p-AKT) were examined using western blot analysis. The influence of celecoxib on IGF-binding protein-3 (IGFBP-3) expression was analyzed using ELISA. Celecoxib inhibited IGF-1-stimulated growth and invasion in a dose-dependent manner. Celecoxib also reduced the expression of IGF-1R, IGFBP-3 and phosphorylation of AKT. The results suggest that modulating the IGF axis may be a new mechanism for the anticancer effect of celecoxib on NSCLC.

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“…The expression of COX-2 may be upregulated in cancer cells or during the inflammatory response. Most significantly, COX-2 inhibitors repress tumor development in the lungs of cancer-treated mice [12]. It is also worth noting that the upregulation of COX-2 expression induced by a variety of stimuli was involved in the activation of the p38 MAPK and ERK pathways in A549 [33][34][35].…”

Section: Discussionmentioning

confidence: 94%

“…Preclinical studies suggest that treatment with a selective COX-2 inhibitor may enhance the antitumor effects of chemotherapy [10,11]. Perioperative COX-2 inhibition could reduce tumor cell adhesion and the metastatic potential of circulating tumor cells in non-small cell lung cancer [12].…”

Section: Introductionmentioning

confidence: 99%

Redox Factor-1 Inhibits Cyclooxygenase-2 Expression via Inhibiting of p38 MAPK in the A549 Cells

Yoo

Kim

Lee

et al. 2010

Korean J Physiol Pharmacol

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Perioperative cyclooxygenase 2 inhibition to reduce tumor cell adhesion and metastatic potential of circulating tumor cells in non–small cell lung cancer

Cited by 23 publications

References 34 publications

Inhibition of the Biosynthesis of Prostaglandin E2 By Low-Dose Aspirin: Implications for Adenocarcinoma Metastasis

Inhibition of the Biosynthesis of Prostaglandin E2 By Low-Dose Aspirin: Implications for Adenocarcinoma Metastasis

Celecoxib inhibits insulin-like growth factor 1 induced growth and invasion in non-small cell lung cancer

Redox Factor-1 Inhibits Cyclooxygenase-2 Expression via Inhibiting of p38 MAPK in the A549 Cells

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