Etodolac, a Selective Cyclooxygenase-2 Inhibitor, Induces Upregulation of E-Cadherin and Has Antitumor Effect on Human Bladder Cancer Cells In Vitro and In Vivo

Okamoto, Akira; Shirakawa, Toshiro; Bito, Toshinori; Shigemura, Katsumi; Hamada, Katsuyuki; Gotoh, Akinobu; Fujisawa, Masato; Kawabata, Masato

doi:10.1016/j.urology.2007.09.061

Cited by 41 publications

(31 citation statements)

References 26 publications

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“…These results provide evidence that etodolac would not suppress the antitumor activity of paclitaxel. Furthermore, the slight antiproliferative effect of etodolac and its enhancement of the antiproliferative effect of paclitaxel in MDA-MB-468 cells observed in the present study is consistent with results of other basic studies showing that etodolac has antineoplastic effects against a variety (Kolluri et al, 2005;Khwaja et al, 2009), bladder (Okamoto et al, 2008), skin (Kapadia et al, 2010), and tongue carcinoma (Mishima et al, 2005), hepatoma (Behari et al, 2007), and pancreatic (Adachi et al, 2008) and blood cancer (Yasui et al, 2005;de Souza Thiago et al, 2009), as well as antimetastatic effects (Iwata et al, 2007;Benish et al, 2008;Tachimori et al, 2008). In addition, a clinical study showed that etodolac can provide secondary prevention of gastric cancer (Yanaoka et al, 2010).…”

Section: Discussionsupporting

confidence: 92%

Etodolac, a Cyclooxygenase-2 Inhibitor, Attenuates Paclitaxel-Induced Peripheral Neuropathy in a Mouse Model of Mechanical Allodynia

Ito¹,

Tajima²,

Nogawa³

et al. 2012

J Pharmacol Exp Ther

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The effect of the cyclooxygenase-2 (COX-2) inhibitor etodolac on the mechanical allodynia induced by paclitaxel was investigated in mice and compared with the effects of the nonselective COX inhibitors indomethacin and diclofenac, the selective COX-2 inhibitor celecoxib, the calcium channel ␣ 2 ␦ subunit inhibitor pregabalin, the sodium channel blocker mexiletine, and the serotonin-norepinephrine reuptake inhibitor duloxetine. The decrease in the paw-withdrawal threshold induced by paclitaxel was reversed by oral administration of etodolac at 10 mg/kg but was not affected by indomethacin, diclofenac, or celecoxib. The antiallodynic effect of etodolac gradually increased during repeated administration, and after 2 weeks the paw-withdrawal threshold at the preadministration point was significantly increased. Pregabalin, duloxetine, and mexiletine also showed an antiallodynic effect in this model. Whereas pregabalin had a preadministration effect similar to that of etodolac during repeated administration, mexiletine or duloxetine had no such effect. There was almost no difference in the distribution of etodolac and diclofenac in nervous tissue, indicating that COX inhibition is unlikely to be involved in the antiallodynic effect of etodolac. Etodolac did not show a neuroprotective effect against morphological transformations such as the axonal degeneration induced by paclitaxel. Instead, etodolac probably acts at the level of functional changes accompanying paclitaxel treatment, such as alterations in the activation state of components of the pain transmission pathway. Our findings suggest that etodolac attenuates paclitaxel-induced peripheral neuropathy by a COX-independent pathway and that it might be useful for the treatment of paclitaxel-induced peripheral neuropathy.

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Section: Discussionsupporting

confidence: 92%

Etodolac, a Cyclooxygenase-2 Inhibitor, Attenuates Paclitaxel-Induced Peripheral Neuropathy in a Mouse Model of Mechanical Allodynia

Ito¹,

Tajima²,

Nogawa³

et al. 2012

J Pharmacol Exp Ther

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“…Higher COX-2 expression which was detected in specimens with perineurial and lymphatic invasion also supported the role of this marker in cell motility and invasion via down-modulation of some adhesion molecules and activation of matrix metalloproteinases (Pruthi et al, 2004;Meric et al, 2006). According to the expression of COX-2 in our patients and the previous reports on the effective role of selective COX-2 inhibitors in human bladder cancer (Pruthi et al, 2004;Okamoto et al, 2008;Dhawan et al, 2010), this marker could be a valuable biological target in the evaluation and treatment of patients with bladder TCC.…”

Section: Discussionsupporting

confidence: 86%

“…Some authors also revealed that the expression of this marker was associated with higher grade and stage of bladder tumor (Matsuzawa et al, 2002;Wadhwa et al, 2005;Jang and Lee, 2009). Moreover, several studies suggest the effective role of selective COX-2 inhibitors in human bladder cancer (Pruthi, 2004;Okamoto et al, 2008;Dhawan et al, 2010). Zhu et al (2012) reviewed the publications about the influence and activation of inflammatory mediators including Cox-2 in bladder cancer and emphasis on the potential role of therapeutic targets.…”

Section: Cyclooxygenase-2 Expression In Urinary Bladder Transitional mentioning

confidence: 99%

Cyclooxygenase-2 Expression in Urinary Bladder Transitional Cell Carcinoma and its Association with Clinicopathological Characteristics

Tabriz

Olfati²,

Ahmadi³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…Recent studies have proved that ET has antitumor effect on different human cancer cells [31,32]. ET is one of the selective COX-2 inhibitors; it possesses 10-fold COX-2 selectivity over COX-1 [32,33].…”

Section: Introductionmentioning

confidence: 99%

Nanosuspension: An Emerging Trend for Bioavailability Enhancement of Etodolac

Afifi

Hassan

Elkhodairy

2015

International Journal of Polymer Science

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Etodolac (ET) (poorly soluble drug) nanosuspensions were prepared by both pH shift method and antisolvent techniques in order to increase its dissolution rate. Various stabilizers were used, namely, Tween 20 and 80, HPMC, PVP K44, PVA, PEG 400, NaCMC, and -cyclodextrin. The prepared nanosuspensions were characterized by Fourier transform infrared spectroscopy (FTIR) and scanning electron microscope (SEM) and evaluated for their particle size, particle size distribution, and in vitro dissolution rate. In general, it was found that the antisolvent method for the preparation of ET nanosuspensions reduced the drug particle size to a higher extent compared to the pH shift method. The dissolution rate of ET in distilled water was markedly enhanced in the nanosized system, as more than 65% of drug dissolved in 10 min from all the nanosuspension formulations except F5 (stabilized with PVP K44) and F8 (stabilized with Tween 20), as compared to less than 20% of crude drug. Nanoparticles prepared by antisolvent method using Tween 80 as a stabilizer were selected for further in vivo study. The in vivo test demonstrated that nanoparticles of ET were well absorbed with a percentage drug absorption value 2.7 times more than that of micrometric size of crude ET.

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Etodolac, a Selective Cyclooxygenase-2 Inhibitor, Induces Upregulation of E-Cadherin and Has Antitumor Effect on Human Bladder Cancer Cells In Vitro and In Vivo

Cited by 41 publications

References 26 publications

Etodolac, a Cyclooxygenase-2 Inhibitor, Attenuates Paclitaxel-Induced Peripheral Neuropathy in a Mouse Model of Mechanical Allodynia

Etodolac, a Cyclooxygenase-2 Inhibitor, Attenuates Paclitaxel-Induced Peripheral Neuropathy in a Mouse Model of Mechanical Allodynia

Cyclooxygenase-2 Expression in Urinary Bladder Transitional Cell Carcinoma and its Association with Clinicopathological Characteristics

Nanosuspension: An Emerging Trend for Bioavailability Enhancement of Etodolac

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