PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29541415-2 2018 We found that NSAIDs including celecoxib (CCB) and ibuprofen (IBU) significantly potentiated the cytotoxicity of Hsp90 inhibitors in human multidrug-resistant (MDR) cells expressing high levels of mutant p53 (mutp53) protein and P-glycoprotein (P-gp), and reversed Hsp90 inhibitor resistance caused by activation of heat shock factor 1 (HSF1) and by up-regulation of heat shock proteins (Hsps) and P-gp. Celecoxib 31-40 ATP binding cassette subfamily B member 1 Homo sapiens 229-243 29541237-10 2018 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. Celecoxib 179-188 ATP binding cassette subfamily B member 1 Homo sapiens 146-150 29541415-3 2018 Inhibition of Akt/mTOR and STAT3 pathways by CCB induced autophagy, which promoted the degradation of mutp53, one of Hsp90 client proteins, and subsequently down-regulated HSF1/Hsps and P-gp. Celecoxib 45-48 ATP binding cassette subfamily B member 1 Homo sapiens 186-190 29541415-5 2018 Furthermore, CCB and IBU suppressed Hsp90 inhibitor-induced HSF1/Hsp70/P-gp activity and mutp53 expression in MDR cells. Celecoxib 13-16 ATP binding cassette subfamily B member 1 Homo sapiens 71-75 29541415-2 2018 We found that NSAIDs including celecoxib (CCB) and ibuprofen (IBU) significantly potentiated the cytotoxicity of Hsp90 inhibitors in human multidrug-resistant (MDR) cells expressing high levels of mutant p53 (mutp53) protein and P-glycoprotein (P-gp), and reversed Hsp90 inhibitor resistance caused by activation of heat shock factor 1 (HSF1) and by up-regulation of heat shock proteins (Hsps) and P-gp. Celecoxib 31-40 ATP binding cassette subfamily B member 1 Homo sapiens 245-249 29541415-2 2018 We found that NSAIDs including celecoxib (CCB) and ibuprofen (IBU) significantly potentiated the cytotoxicity of Hsp90 inhibitors in human multidrug-resistant (MDR) cells expressing high levels of mutant p53 (mutp53) protein and P-glycoprotein (P-gp), and reversed Hsp90 inhibitor resistance caused by activation of heat shock factor 1 (HSF1) and by up-regulation of heat shock proteins (Hsps) and P-gp. Celecoxib 31-40 ATP binding cassette subfamily B member 1 Homo sapiens 398-402 29541415-2 2018 We found that NSAIDs including celecoxib (CCB) and ibuprofen (IBU) significantly potentiated the cytotoxicity of Hsp90 inhibitors in human multidrug-resistant (MDR) cells expressing high levels of mutant p53 (mutp53) protein and P-glycoprotein (P-gp), and reversed Hsp90 inhibitor resistance caused by activation of heat shock factor 1 (HSF1) and by up-regulation of heat shock proteins (Hsps) and P-gp. Celecoxib 42-45 ATP binding cassette subfamily B member 1 Homo sapiens 229-243 29541415-2 2018 We found that NSAIDs including celecoxib (CCB) and ibuprofen (IBU) significantly potentiated the cytotoxicity of Hsp90 inhibitors in human multidrug-resistant (MDR) cells expressing high levels of mutant p53 (mutp53) protein and P-glycoprotein (P-gp), and reversed Hsp90 inhibitor resistance caused by activation of heat shock factor 1 (HSF1) and by up-regulation of heat shock proteins (Hsps) and P-gp. Celecoxib 42-45 ATP binding cassette subfamily B member 1 Homo sapiens 245-249 29541415-2 2018 We found that NSAIDs including celecoxib (CCB) and ibuprofen (IBU) significantly potentiated the cytotoxicity of Hsp90 inhibitors in human multidrug-resistant (MDR) cells expressing high levels of mutant p53 (mutp53) protein and P-glycoprotein (P-gp), and reversed Hsp90 inhibitor resistance caused by activation of heat shock factor 1 (HSF1) and by up-regulation of heat shock proteins (Hsps) and P-gp. Celecoxib 42-45 ATP binding cassette subfamily B member 1 Homo sapiens 398-402 28053596-8 2017 RESULTS: MDR1, MRP1, BCRP and Trkb, E-cadherin, beta-catenin were significantly downregulated in cells treated with the combination of celecoxib and cisplatin, and decreased beta-catenin level was found in cells with wortmannin, a specific PI3K inhibitor. Celecoxib 135-144 ATP binding cassette subfamily B member 1 Homo sapiens 9-13 26407653-2 2015 The present study was to explore the correlation of celecoxib, a cyclooxygenase-2 specific inhibitor, and P-glycoprotein in drug-resistant gastric cancer cells. Celecoxib 52-61 ATP binding cassette subfamily B member 1 Homo sapiens 106-120 27798865-0 2016 Co-treatment with Celecoxib or NS398 Strongly Sensitizes Resistant Cancer Cells to Antimitotic Drugs Independent of P-gp Inhibition. Celecoxib 18-27 ATP binding cassette subfamily B member 1 Homo sapiens 116-120 26407653-5 2015 Further studies revealed down-regulation of cyclooxygenase-2 and P-glycoprotein expression by celecoxib, and a decline in prostaglandin E2 release and protein kinase A level. Celecoxib 94-103 ATP binding cassette subfamily B member 1 Homo sapiens 65-79 25736380-5 2015 In vivo OSU-03012/sildenafil was more efficacious than treatment with celecoxib and sildenafil at killing tumor cells without damaging normal tissues and in parallel reduced expression of ABCB1 and ABCG2 in the normal brain. Celecoxib 70-79 ATP binding cassette subfamily B member 1 Homo sapiens 188-193 26417912-3 2015 In a dose dependent fashion celecoxib enhanced the ability of [sorafenib + sildenafil] to reduce expression of multiple chaperone proteins in parallel with lower levels of the drug efflux pumps ABCB1 and ABCG2. Celecoxib 28-37 ATP binding cassette subfamily B member 1 Homo sapiens 194-199 25916699-3 2015 Our previous studies have highlighted the role of cyclooxygenase-2 (COX-2) in regulating the expression of multidrug resistant protein-1 (MDR1), P-gp, in imatinib-resistant K562 cells (IR-K562) via PGE2-cAMP-PKC-NF-kappaB pathway and inhibition of COX-2 by celecoxib, a COX-2 specific inhibitor, inhibits this pathway and reverses the drug resistance. Celecoxib 257-266 ATP binding cassette subfamily B member 1 Homo sapiens 107-136 25916699-3 2015 Our previous studies have highlighted the role of cyclooxygenase-2 (COX-2) in regulating the expression of multidrug resistant protein-1 (MDR1), P-gp, in imatinib-resistant K562 cells (IR-K562) via PGE2-cAMP-PKC-NF-kappaB pathway and inhibition of COX-2 by celecoxib, a COX-2 specific inhibitor, inhibits this pathway and reverses the drug resistance. Celecoxib 257-266 ATP binding cassette subfamily B member 1 Homo sapiens 138-142 25691007-8 2015 Low and moderate concentrations of celecoxib modulate the expression of iNOS and P-gp in mitochondria of MDR cancer cells independently from inhibition of COX-2 activity. Celecoxib 35-44 ATP binding cassette subfamily B member 1 Homo sapiens 81-85 23803204-9 2013 CONCLUSIONS: Celecoxib enhances the chemosensitivity of KB/VCR cells by down-regulating P-gp expression, which is partially mediated by modification of cyclin D1 and p21(WAF1/CIP1) to result in cell cycle arrest. Celecoxib 13-22 ATP binding cassette subfamily B member 1 Homo sapiens 88-92 23991582-1 2013 OBJECTIVE: To investigate the influence of celecoxib, cycloxygenase-2 (COX-2) selective inhibitor, upon the proliferation of KB/VCR cells, and analyze the effect of celecoxib on the expression of P-glycoprotein (P-gp). Celecoxib 43-52 ATP binding cassette subfamily B member 1 Homo sapiens 196-210 23991582-1 2013 OBJECTIVE: To investigate the influence of celecoxib, cycloxygenase-2 (COX-2) selective inhibitor, upon the proliferation of KB/VCR cells, and analyze the effect of celecoxib on the expression of P-glycoprotein (P-gp). Celecoxib 43-52 ATP binding cassette subfamily B member 1 Homo sapiens 212-216 23991582-7 2013 The expression of P-gp in Celecoxib + VCR group and Celecoxib group were markedly lower, compared with those in VCR group and Celecoxib + VCR + PGE2 group (P < 0.01). Celecoxib 26-35 ATP binding cassette subfamily B member 1 Homo sapiens 18-22 23991582-7 2013 The expression of P-gp in Celecoxib + VCR group and Celecoxib group were markedly lower, compared with those in VCR group and Celecoxib + VCR + PGE2 group (P < 0.01). Celecoxib 52-61 ATP binding cassette subfamily B member 1 Homo sapiens 18-22 23991582-7 2013 The expression of P-gp in Celecoxib + VCR group and Celecoxib group were markedly lower, compared with those in VCR group and Celecoxib + VCR + PGE2 group (P < 0.01). Celecoxib 52-61 ATP binding cassette subfamily B member 1 Homo sapiens 18-22 23991582-12 2013 The mechanism probably correlates with the downregulation of celecoxib on the expression of P-gp and the increase of apoptosis. Celecoxib 61-70 ATP binding cassette subfamily B member 1 Homo sapiens 92-96 22904679-7 2012 Given the dramatic response to a combination of celecoxib + 5-FU, the possibility that celecoxib may modulate chemosensitivity as a result of its ability to inhibit MDR-1 was examined. Celecoxib 87-96 ATP binding cassette subfamily B member 1 Homo sapiens 165-170 19685055-0 2010 Celecoxib inhibits MDR1 expression through COX-2-dependent mechanism in human hepatocellular carcinoma (HepG2) cell line. Celecoxib 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 19-23 20937780-2 2011 Accumulating evidence suggests that the cyclooxygenase-2 (COX-2)-specific inhibitor celecoxib would not only inhibit COX-2 but also help in the reversal of drug resistance in cancers by inhibiting the MDR1 efflux pump. Celecoxib 84-93 ATP binding cassette subfamily B member 1 Homo sapiens 201-205 20229271-9 2011 After co-incubation with both the same dose of doxorubicin and 10 muM celecoxib for 7 days, both mRNA level and protein level of MDR1, c-Jun and NF-kappaB up-regulated by doxorubicin were partly reversed (P < 0.01); DNA-binding activity of nuclear transcription factors AP-1 and NF-kappaB were inhibited; and the function of P-gp was decreased (P < 0.01). Celecoxib 70-79 ATP binding cassette subfamily B member 1 Homo sapiens 129-133 20229271-9 2011 After co-incubation with both the same dose of doxorubicin and 10 muM celecoxib for 7 days, both mRNA level and protein level of MDR1, c-Jun and NF-kappaB up-regulated by doxorubicin were partly reversed (P < 0.01); DNA-binding activity of nuclear transcription factors AP-1 and NF-kappaB were inhibited; and the function of P-gp was decreased (P < 0.01). Celecoxib 70-79 ATP binding cassette subfamily B member 1 Homo sapiens 328-332 20229271-11 2011 CONCLUSION: Celecoxib effectively prevents the development of chemoresistance in breast cancer cell line MCF-7 induced by doxorubicin, which was partly involved in inhibiting the expression and DNA-binding activity of nuclear transcription factors AP-1 and NF-kappaB and downstream expression and function of P-gp. Celecoxib 12-21 ATP binding cassette subfamily B member 1 Homo sapiens 309-313 22305971-2 2012 We found that celecoxib induced apoptosis in TT cells and decreased drug efflux by reducing the expression of MDR-1 mRNA, which codes for the drug efflux pump P-gp. Celecoxib 14-23 ATP binding cassette subfamily B member 1 Homo sapiens 110-115 21835258-0 2012 The COX-2 inhibitor Celecoxib enhances the sensitivity of KB/VCR oral cancer cell lines to Vincristine by down-regulating P-glycoprotein expression and function. Celecoxib 20-29 ATP binding cassette subfamily B member 1 Homo sapiens 122-136 21835258-3 2012 Using the MTT method, we investigated the influence of the COX-2 selective inhibitor Celecoxib on the proliferation of KB/VCR oral cancer cell lines and analyzed the effect of Celecoxib on the regulation of P-glycoprotein (P-gp) expression and function. Celecoxib 176-185 ATP binding cassette subfamily B member 1 Homo sapiens 207-221 21835258-9 2012 P-gp expression levels in KB/KBV cells treated with Celecoxib plus VCR (10 mumol/L+1.5 mumol/L, respectively) were markedly lower than the levels in control cells and those treated with VCR (1.5 mumol/L) (all P<0.01). Celecoxib 52-61 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 21835258-11 2012 The underlying mechanism of these phenomena is likely correlated with the down-regulation of the expression and function of P-gp due to Celecoxib, thereby increasing the amount of VCR accumulated in KB/VCR cells. Celecoxib 136-145 ATP binding cassette subfamily B member 1 Homo sapiens 124-128 19685055-3 2010 The induction of MDR1 expression by PGE2 and its downregulation by celecoxib or by COX-2 knockdown suggests that the enhanced sensitivity of HepG2 cells to doxorubicin by celecoxib is mediated by the downregulation of MDR1 expression, through COX-2-dependent mechanism. Celecoxib 67-76 ATP binding cassette subfamily B member 1 Homo sapiens 17-21 19685055-3 2010 The induction of MDR1 expression by PGE2 and its downregulation by celecoxib or by COX-2 knockdown suggests that the enhanced sensitivity of HepG2 cells to doxorubicin by celecoxib is mediated by the downregulation of MDR1 expression, through COX-2-dependent mechanism. Celecoxib 171-180 ATP binding cassette subfamily B member 1 Homo sapiens 17-21 19685055-4 2010 Further studies revealed the involvement of AP-1 in the celecoxib-induced downregulation of MDR1 expression. Celecoxib 56-65 ATP binding cassette subfamily B member 1 Homo sapiens 92-96 19426390-10 2009 The inhibition of P-gp could be achieved with celecoxib alone and combination with octreotide (0.486 +/- 0.012, 0.252 +/- 0.014 vs 0.941 +/- 0.033, P < 0.05). Celecoxib 46-55 ATP binding cassette subfamily B member 1 Homo sapiens 18-22 19562670-0 2009 Celecoxib enhanced the sensitivity of cancer cells to anticancer drugs by inhibition of the expression of P-glycoprotein through a COX-2-independent manner. Celecoxib 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 106-120 19562670-9 2009 Enzyme activity and methylation analyses demonstrated that the inhibitory effect of celecoxib on p170 was independent on COX-2 but closely related to hypermethylation of MDR1 gene promoter. Celecoxib 84-93 ATP binding cassette subfamily B member 1 Homo sapiens 170-174 19447220-3 2009 Here we show that P-glycoprotein (P-gp) mediates cell-cycle arrest and autophagy induced by celecoxib in human MDR overexpressing hepatocellular carcinoma cell line by down-regulation of the HGF/MET autocrine loop and Bcl-2 expression. Celecoxib 92-101 ATP binding cassette subfamily B member 1 Homo sapiens 18-32 19447220-3 2009 Here we show that P-glycoprotein (P-gp) mediates cell-cycle arrest and autophagy induced by celecoxib in human MDR overexpressing hepatocellular carcinoma cell line by down-regulation of the HGF/MET autocrine loop and Bcl-2 expression. Celecoxib 92-101 ATP binding cassette subfamily B member 1 Homo sapiens 34-38 18083230-8 2008 Further studies revealed down-regulation of MDR-1 by celecoxib and a decline in p-Akt levels. Celecoxib 53-62 ATP binding cassette subfamily B member 1 Homo sapiens 44-49 18083230-11 2008 In conclusion, the present study indicates over-expression of COX-2 and MDR-1 in IR-K562 cells and celecoxib, a COX-2 specific inhibitor, induces apoptosis by inhibiting COX-2 and down-regulating MDR-1 expression through Akt/p-Akt signaling pathway. Celecoxib 99-108 ATP binding cassette subfamily B member 1 Homo sapiens 196-201 31623608-3 2019 Celecoxib (CXB), a selective COX-2 inhibitor, can dramatically enhance the cytotoxicity of doxorubicin (DOX) in breast cancer cells overexpressing P-gp. Celecoxib 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 147-151 31623608-3 2019 Celecoxib (CXB), a selective COX-2 inhibitor, can dramatically enhance the cytotoxicity of doxorubicin (DOX) in breast cancer cells overexpressing P-gp. Celecoxib 11-14 ATP binding cassette subfamily B member 1 Homo sapiens 147-151 17704658-0 2007 Effects of celecoxib on the reversal of multidrug resistance in human gastric carcinoma by downregulation of the expression and activity of P-glycoprotein. Celecoxib 11-20 ATP binding cassette subfamily B member 1 Homo sapiens 140-154 17704658-1 2007 We investigated the effects of celecoxib on the cell proliferation and the expression and activity of P-glycoprotein in the human gastric carcinoma multidrug resistance sublines SGC7901/adriamycin and SGC7901/vincristine. Celecoxib 31-40 ATP binding cassette subfamily B member 1 Homo sapiens 102-116 17704658-8 2007 P-glycoprotein expression levels in the two multidrug resistance sublines treated with celecoxib were significantly lower than those in control groups, 0.28 vs. 0.71 in the SGC7901/adriamycin subline and 0.21 vs. 0.83 in the SGC7901/vincristine subline, respectively, P<0.05. Celecoxib 87-96 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 17510421-0 2007 P-glycoprotein mediates celecoxib-induced apoptosis in multiple drug-resistant cell lines. Celecoxib 24-33 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 17510421-3 2007 Because COX-2 induces P-glycoprotein expression, we evaluated the effect of celecoxib, a specific inhibitor of COX-2 activity, on P-glycoprotein-mediated resistance to apoptosis in cell lines expressing multidrug resistant (MDR) phenotype. Celecoxib 76-85 ATP binding cassette subfamily B member 1 Homo sapiens 130-144 17510421-5 2007 We found that 10 micromol/L celecoxib reduced P-glycoprotein, Bcl-x(L), and Bcl-2 expression, and induced translocation of Bax from cytosol to mitochondria and cytochrome c release into cytosol in MDR-positive hepatocellular carcinoma cells. Celecoxib 28-37 ATP binding cassette subfamily B member 1 Homo sapiens 46-60 17510421-8 2007 Interestingly, although inhibiting COX-2 activity, 50 micromol/L celecoxib weakly increased the expression of COX-2 and P-glycoprotein and did not alter Bcl-x(L) and Bcl-2 expression. Celecoxib 65-74 ATP binding cassette subfamily B member 1 Homo sapiens 120-134 17510421-10 2007 This effect is mediated by P-glycoprotein and suggests that the efficacy of celecoxib in the treatment of different types of cancer may depend on celecoxib concentration and P-glycoprotein expression. Celecoxib 76-85 ATP binding cassette subfamily B member 1 Homo sapiens 27-41 17510421-10 2007 This effect is mediated by P-glycoprotein and suggests that the efficacy of celecoxib in the treatment of different types of cancer may depend on celecoxib concentration and P-glycoprotein expression. Celecoxib 76-85 ATP binding cassette subfamily B member 1 Homo sapiens 174-188 17510421-10 2007 This effect is mediated by P-glycoprotein and suggests that the efficacy of celecoxib in the treatment of different types of cancer may depend on celecoxib concentration and P-glycoprotein expression. Celecoxib 146-155 ATP binding cassette subfamily B member 1 Homo sapiens 27-41 11915030-8 2002 CLX and NIME also inhibited cell proliferation, but only in MDR1 cells. Celecoxib 0-3 ATP binding cassette subfamily B member 1 Homo sapiens 60-64