Celecoxib enhances doxorubicin-induced cytotoxicity in MDA-MB231 cells by NF-κB-mediated increase of intracellular doxorubicin accumulation

Wijngaarden, Jens van; Beek, Ermond van; Rossum, Gerda van; Bent, Chris van der; Hoekman, K.; Pluijm, Gabri van der; Pol, M.A. van der; Broxterman, Henk J.; Hinsbergh, Victor W.M. van; Löwik, Clemens W.G.M.

doi:10.1016/j.ejca.2006.09.010

Cited by 70 publications

(58 citation statements)

References 39 publications

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“…We have demonstrated that regulation of Cox-2 by Akt is also mediated via NF-kB in endometrial cancer cells (St Germain et al 2004b). Knockdown of Cox-2 expression by shRNA or by using Cox-2 inhibitors (celecoxib) was also tested and showed potent antitumor activity and chemosensitization activity to taxanes in laryngeal cancer (Wang et al 2008) and to doxorubicin in breast cancer (van Wijngaarden et al 2007, Singh et al 2008. Similar relationship between Cox-2 expression and chemosensitivity to cisplatin has also been investigated in colon cancer cell lines using selective Cox-2 inhibitor JTE-522 (Saikawa et al 2004) and this hypothesis can also be tested in endometrial cancer, since Cox-2 has been shown to be involved in the development and progression of endometrial cancer (Ohno et al 2005).…”

Section: Cyclooxygenases and Prostaglandinsmentioning

confidence: 99%

Resistance to chemotherapy and hormone therapy in endometrial cancer

Chaudhry¹,

Asselin²

2009

Endocrine-Related Cancer

111

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Endometrial cancer is the most common gynecological malignancy in developed countries and represents the eighth leading cause of cancer related death in women. The growing incidence of endometrial cancer leads scientists and oncologists to identify effective preventive measures and also molecular markers for diagnosis and prognosis. Chemotherapy and hormone therapy is the mainstay treatment option for advanced and recurrent endometrial cancer and response to therapy is one of the most important factor which favors prognosis and overall survival. In recent years, there have been major advances in the treatment of patients with endometrial cancer. Despite advances made in the treatment of this cancer, the overall survival of patients has not significantly improved because considerable number of patients harbor tumor refractory to these therapies and the majority of the initially responsive tumors become refractory to treatments. Therefore, determination of sensitivity/resistance is becoming increasingly important for individualization of endometrial cancer therapy. The aim of this review is to present the existing knowledge about the molecular markers that could play a crucial role in determining resistance to chemo-and hormone therapy. Extensive literature search for the cell signaling pathways and factors responsible for chemoresistance have been performed and reviewed. Several recent studies suggest that deregulations in the apoptotic pathways (such as p53, Fas/FasL, Bcl-2 family proteins, inhibitor of apoptosis proteins), survival pathways (PI3K/AKT, MAPK), hormone receptor signaling pathways (progesterone receptor), Cyclooxygenase-2 and Her-2 are considered as key factors involved in the onset and maintenance of therapeutic resistance, suggesting that resistance is a multi-factorial phenomenon.

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Section: Cyclooxygenases and Prostaglandinsmentioning

confidence: 99%

Resistance to chemotherapy and hormone therapy in endometrial cancer

Chaudhry¹,

Asselin²

2009

Endocrine-Related Cancer

111

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“…After 10 days, animals having a tumor with a volume (TV) of 20 ± 3 mm 3 were selected and randomly divided into four groups of eight mice each. TV was assessed by using a caliper to measure the axes and calculated by the formula TV = π/6 (d1 x d2) 1/2 (Van Wijngaarden et al, 2007). Mice (8 per experimental group) were injected intraperitoneally with control (DMSO), meloxicam (15 mg/kg), doxorubicin (0.5 mg/kg), or a combination of meloxicam and doxorubicin in a total volume of 100 μL according to previous results (data not shown).…”

Section: Animal Studymentioning

confidence: 99%

“…Experimental studies reported that NSAIDs and specific COX-2 inhibitors inhibited cell proliferation, cell motility, adhesion, angiogenesis, and the induction of apoptosis in tumors (Gately and Li, 2004). These anticancer properties suggest the potential for a treatment strategy that combines NSAIDs and COX-2 inhibitors with conventional anticancer therapies, such as chemotherapy (van Wijngaarden et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

“…The doxorubicin accumulation in the A549 cell assay was as described by van Wijngaarden et al (2007), with slight modifications. Briefly, A549 cells were incubated for 24 h in medium containing doxorubicin (0.5, 1, or 5 μM), with or without meloxicam (50 μM), or celecoxib (50 μM).…”

Section: Doxorubicin Accumulation Assaymentioning

confidence: 99%

“…There is a suggestion that the COX-inhibitors modulate the resistance of tumors to chemotherapeutic drugs by affecting the activity of plasma membrane transporter proteins of the ABC-transporter family, which behave as energydependent efflux pumps for cytostatics (van Wijngaarden et al, 2007). There are three key mammalian transporters involved in the transport of most anticancer agents: P-glycoprotein (P-gp/ABCB1), multidrug-resistance protein-1 (MRP1/ABCC1), and breast cancer resistance protein (BCRP/ABCC2) (Sparreboom et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

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Meloxicam increases intracellular accumulation of doxorubicin via downregulation of multidrug resistance-associated protein 1 (MRP1) in A549 cells

Chen

Zhang

2015

Genet. Mol. Res.

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ABSTRACT. It has been suggested that selected COX inhibitors can overcome multidrug resistance through the inhibition of ATP-binding cassette-transporter proteins thereby enhancing the inhibitory effect of doxorubicin on human tumor growth and promoting the actions of cytostatics. However, their effect on lung cancer and the molecular mechanisms involved in the overcoming of multidrug resistance are unclear. In the present study, the ability of meloxicam, a COX-2-specific inhibitor to enhance doxorubicin-mediated inhibition was investigated in human A549 lung cancer in vivo and in vitro. In order to unravel the molecular mechanisms involved in doxorubicin accumulation, we measured the levels of multidrug resistance-associated protein (MRP)-transporter protein activity and expression by western blotting, since this has been implicated in meloxicam action as well as in chemoresistance. We found that, in A549 cells, meloxicam could increase intracellular accumulation of doxorubicin, a substrate for MRP, through inhibition of cellular export. Western blot analysis indicated that meloxicam reduced 14549 COX-2 inhibitor as a lung cancer therapeutic ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (4): 14548-14560 (2015) the expression of MRP1 and MRP4. The results reported in the present study demonstrate for the first time that the specific COX-2 inhibitor meloxicam can increase the intracellular accumulation of doxorubicin and enhance doxorubicin-induced cytotoxicity in A549 cancer cells by reducing the expression of MRP1 and MRP4.

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Chitosan as Anticancer Compound and Nanoparticulate Matrix for Cancer Therapeutics

Nawaz

Wong

2020

Encyclopedia of Marine Biotechnology

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Celecoxib enhances doxorubicin-induced cytotoxicity in MDA-MB231 cells by NF-κB-mediated increase of intracellular doxorubicin accumulation

Cited by 70 publications

References 39 publications

Resistance to chemotherapy and hormone therapy in endometrial cancer

Resistance to chemotherapy and hormone therapy in endometrial cancer

Meloxicam increases intracellular accumulation of doxorubicin via downregulation of multidrug resistance-associated protein 1 (MRP1) in A549 cells

Chitosan as Anticancer Compound and Nanoparticulate Matrix for Cancer Therapeutics

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