Imatinib-resistant K562 cells are more sensitive to celecoxib, a selective COX-2 inhibitor: Role of COX-2 and MDR-1

Arunasree, Kalle M.; Roy, Kunal; Anilkumar, Kotha; Aparna, A.; Reddy, Gorla V.; Reddanna, Pallu

doi:10.1016/j.leukres.2007.11.007

Cited by 63 publications

(41 citation statements)

References 49 publications

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“…33) In addition, the involvement of COX-2 in the development of resistance to imatinib was found in K562 cells. 34) These papers were suggesting that PGE2 may serve as a downstream effector of imatinib. PGs are known to be potent regulators of the electrical and mechanical activities of GI smooth muscle.…”

Section: Discussionmentioning

confidence: 99%

Effects of Imatinib Mesylate in Interstitial Cells of Cajal from Murine Small Intestine

Kim

Chae

Kwon

et al. 2010

Biological & Pharmaceutical Bulletin

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The interstitial cells of Cajal (ICCs) are pacemakers in the gastrointestinal tract. The possibility of whether imatinib mesylate, a Kit receptor tyrosine kinase inhibitor, modulates pacemaker activities in the ICC was examined using the whole cell patch clamp technique. Imatinib decreased the amplitude of pacemaker potentials in a dose-dependent manner in current-clamp mode. Because the effects of imatinib on pacemaker potentials were the same as those of pinacidil, we examined the effect of glibenclamide on ICC exposed to imatinib. The effects of imatinib on pacemaker potentials were blocked by glibenclamide. To see whether the production of prostaglandins (PGs) is involved in the inhibitory effect of imatinib on pacemaker potentials, we tested the effects of naproxen (a non-selective cyclooxygenase inhibitor) and AH6809 (a prostaglandin EP1 and EP2 receptor antagonist). Naproxen and AH6809 blocked the inhibitory effects of imatinib on ICC. Butaprost (an EP2 receptor agonist) showed the actions on pacemaker potentials in the same manner as imatinib. However, SC 19220 (an EP1 receptor antagonist) has no effects. To investigate the involvement of cAMP and protein kinase A (PKA) in the effects of imatinib on ICC, SQ 22536 (an inhibitor of adenylate cyclase) and mPKAI (an inhibitor of myristoylated PKA) were used. Both SQ-22536 and mPKAI blocked the imatinib-mediated inhibition of pacemaker potentials. However, the protein kinase C (PKC) inhibitors did not block the imatinib-mediated inhibition of pacemaker potentials. These results indicate that imatinib inhibits the pacemaker potentials of ICC by activating ATP-sensitive K ؉ ؉ channels and PKA-dependent, PKC-independent manner.

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Section: Discussionmentioning

confidence: 99%

Effects of Imatinib Mesylate in Interstitial Cells of Cajal from Murine Small Intestine

Kim

Chae

Kwon

et al. 2010

Biological & Pharmaceutical Bulletin

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“…These effects of NSAIDs have been demonstrated in several different malignancies (81)(82)(83)(84)(85). Permeability glycoprotein (P-gp), which acts on a broad substrate range, is one of the most extensively investigated and best characterised transporter proteins.…”

Section: Combination Of Nsaids With Chemotherapeutic Drugs In Vitromentioning

confidence: 99%

Potency of non-steroidal anti-inflammatory drugs in chemotherapy

Hiľovská

Jendželovský

Fedoročko

2014

Molecular and Clinical Oncology

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“…Previous studies have revealed that celecoxib may prevent chemotherapy drug resistance in digestive and gynecologic carcinomas (9)(10)(11)(12), but whether it serves a similar role in T-cell lymphoma has not been determined. The present study demonstrated that celecoxib sensitized Jurkat and Hut-78 cells to various chemotherapy drugs by triggering apoptosis and inhibiting the expression of MDR-associated proteins.…”

Section: Discussionmentioning

confidence: 99%

“…It has been demonstrated previously that the Bcl2 family members protect against the activation of multiple signaling pathways leading to apoptosis of tumor cells, whereas the activation of Bax family members will induce cell apoptosis, indicating that Bcl2/Bax axis played a crucial part in regulating the common apoptosis pathway (8)(9)(10). In the present study, the celecoxib-treated lymphoma cells exhibited significantly decreased expression of Bcl-2 and increased expression of Bax compared with those that were not treated with celecoxib, suggesting that effect on the Bcl-2/BaX protein ratio may be an important contributing factor to celecoxib-induced apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…P65, the primary functioning subunit of activated NF-κB, is an important indicator for predicting MDR in tumors, as it promotes cell viability, causes apoptosis resistance and enhances expression of various MDR-associated proteins including P-gp and MRP1 (7). Furthermore, previous studies have also confirmed that the expression of Bcl-2 may be directly upregulated by activation of the NF-κB signaling pathway, thereby inhibiting Bax expression and leading to an anti-apoptotic effect in tumor cells (8)(9)(10)(11). In the present study, the results suggested that the expression of P65, Bcl2, P-gp and MRP1 was significantly decreased, while the expression of Bax was increased in celecoxib-treated Jurkat and Hut-78 cells t compared with those that were not treated with celecoxib.…”

Section: Discussionmentioning

confidence: 99%

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Celecoxib enhances sensitivity to chemotherapy drugs of T‑cell lymphoma

Yang

Zhao

et al. 2018

Oncol Lett

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Abstract. Celecoxib is a newly-identified nonsteroidal anti-inflammatory drug, which has been used to treat fever in clinical practice. Celecoxib has been demonstrated to suppress the viability of various human tumor cells. However, the effect of celecoxib on response of T-cell lymphoma to chemotherapy agents remains unclear. The aim of the present study was to investigate the effect of celecoxib on chemosensitivity of human T-cell lymphoma, and to address the underlying mechanism of action. The cytotoxicity of CDDP, epirubicin and VCR on Jurkat and Hut-78 cells treated with celecoxib was assessed by MTT assay, and the half-maximal inhibitory concentration (IC 50 ) value was calculated by Origin 75 software. The effect of celecoxib on apoptosis and intracellular concentration of Rhodamine-123 in Jurkat and Hut-78 cells was analyzed by flow cytometry. The expression of transcription factor p65 (p65), B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), multidrug resistance 1 (MDR1) and multidrug resistance-associated protein 1 (MRP1) at mRNA and protein levels were detected by reverse transcription quantitative polymerase chain reaction and western blotting, respectively. Proliferation suppression rates and apoptosis levels were significantly increased in Jurkat and Hut-78 cells combined with celecoxib compared with those without celecoxib, when treated with CDDP, epirubicin and VCR. The IC 50 values of the chemotherapy agents were lower in Jurkat and Hut-78 cells treated with celecoxib compared with those that were not.The apoptosis level, expression of Bax and the intracellular concentration of Rhodamine-123 were increased, whereas the expression of p65, Bcl-2, MDR1 and MRP1 were decreased, in celecoxib-treated Jurkat and Hut-78 cells compared with those without celecoxib treatment. These results indicated that celecoxib may enhance the sensitivity of T-cell lymphoma to chemotherapy drugs by inhibiting the expression of multidrug resistance (MDR)-associated proteins via downregulating the activity of the nuclear factor-κB signaling pathway, suggesting that celecoxib may improve the curative effect of chemotherapy drugs in T-cell lymphoma.

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Imatinib-resistant K562 cells are more sensitive to celecoxib, a selective COX-2 inhibitor: Role of COX-2 and MDR-1

Cited by 63 publications

References 49 publications

Effects of Imatinib Mesylate in Interstitial Cells of Cajal from Murine Small Intestine

Effects of Imatinib Mesylate in Interstitial Cells of Cajal from Murine Small Intestine

Potency of non-steroidal anti-inflammatory drugs in chemotherapy

Celecoxib enhances sensitivity to chemotherapy drugs of T‑cell lymphoma

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