Combination of cyclooxygenase-2 inhibitors and oxaliplatin increases the growth inhibition and death in human colon cancer cells

Lin, Johnson; Hsiao, Po-Wen; Chiu, Ted H.; Ji, Chao

doi:10.1016/j.bcp.2005.05.028

Cited by 69 publications

(55 citation statements)

References 40 publications

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“…Recently, the COX-2 inhibitors etodolac and celecoxib were found to enhance oxaliplatin-induced cytotoxicity in the RKO colorectal cancer cell line, possibly due to associated inhibition of survivin. 33 Such findings are relevant for curcumin in combination with oxaliplatin, since we and others have shown this dietary agent to inhibit both EGFR- 13,34 and COX-2-mediated signaling in tumor-derived cell lines, 35,36 with further potential for synergism through its welldocumented ability to inhibit NF-kB signaling. 37,38 Of primary importance is the lack of systemic toxicity observed so far in phase I clinical trials with very high doses of curcumin, which is in contrast to many therapeutic drugs.…”

Section: Discussionmentioning

confidence: 88%

Comparison of oxaliplatin‐ and curcumin‐mediated antiproliferative effects in colorectal cell lines

Howells

Mitra

Manson

2007

Intl Journal of Cancer

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Colorectal cancer remains a leading cause of cancer death worldwide, despite markedly improved response rates to current systemic therapies. Oxaliplatin either alone or incorporated into 5-fluorouracil/leucovorin regimes has resulted in increased survival rates, particularly with regards to metastatic colorectal carcinoma. The chemopreventive polyphenol curcumin, which is currently in clinical trial, has been advocated for use in colorectal cancer either singly or in combination with chemotherapeutic drugs. In this study, the antiproliferative capacity of both compounds was compared in HCEC (normal-derived), HT29 (p53 mutant adenocarcinoma) and HCT116 (p53wt adenocarcinoma) colorectal cell lines to determine whether effects were cell-type specific at pharmacologically achievable doses, and whether the combination resulted in enhanced efficacy. Both oxaliplatin and curcumin displayed marked antiproliferative capacity at therapeutic concentrations in the two tumor cell lines. Order of sensitivity to oxaliplatin was HCT116>HT29>HCEC, whereas order of sensitivity to curcumin was HT29>HCT116>HCEC. HCT116 cells underwent induction of G2/M arrest in response to both oxaliplatin (irreversible) and curcumin (reversible). Apoptosis was induced by both agents, and up to 16-fold induction of p53 protein was observed in response to the combination. Antiproliferative effects in HT29 cells were largely cell cycle independent, and were mediated by induction of apoptosis. Effects were greatly enhanced in both cell lines when agents were combined. This study provides further evidence that curcumin may be of use in therapeutic regimes directed against colorectal cancer, and suggests that in combination with oxaliplatin it may enhance efficacy of the latter in both p53wt and p53 mutant colorectal tumors. ' 2007 Wiley-Liss, Inc.

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Section: Discussionmentioning

confidence: 88%

Comparison of oxaliplatin‐ and curcumin‐mediated antiproliferative effects in colorectal cell lines

Howells

Mitra

Manson

2007

Intl Journal of Cancer

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“…Phase II trials have also been conducted to test Celecoxib and carboplatin in patients with pretreated recurrent OC, and this approach is yielding promising results (32). In combination with oxaliplatin, Celecoxib has also been shown to inhibit proliferation and tumor growth in colon carcinoma and breast cancer cells (22,33).…”

Section: Discussionmentioning

confidence: 99%

“…NSAIDs have been evaluated as therapies in different types of cancer (23,34,35) and have been shown to have a synergistic effect with known chemotherapeutic agents (31)(32)(33)(36)(37)(38). However, none of these studies have looked specifically at NSAIDs effects on nonproliferating cells.…”

Section: Discussionmentioning

confidence: 99%

NSAIDs induce apoptosis in nonproliferating ovarian cancer cells and inhibit tumor growth in vivo

et al. 2012

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Ovarian cancer (OC) is one of the most lethal gynaecological cancers, which usually has a poor prognosis due to late diagnosis. A large percentage of the OC cell population is in a nonproliferating and quiescent stage, which poses a barrier to success when using most chemotherapeutic agents. Recent studies have shown that several nonsteroidal anti‐inflammatory drugs (NSAIDs) are effective in the treatment of OC. Furthermore, we have previously described the molecular mechanisms of NSAIDs' induction of cancer apoptosis. In this report, we evaluated various structurally distinct NSAIDs for their efficacies in inducing apoptosis in nonproliferating OC cells. Although several NSAIDs‐induced apoptosis, Flufenamic Acid, Flurbiprofen, Finasteride, Celocoxib, and Ibuprofen were the most potent NSAIDs inducing apoptosis. A combination of these agents resulted in an enhanced effect. Furthermore, we demonstrate that the combination of Flurbiprofen, which targets nonproliferative cells, and Sulindac Sulfide, that affects proliferative cells, strongly reduced tumor growth when compared with a single agent treatment. Our data strongly support the hypothesis that drug treatment regimens that target nonproliferating and proliferating cells may have significant efficacy against OC. These results also provide a rationale for employing compounds or even chemically modified NSAIDs, which selectively and efficiently induce apoptosis in cells during different stages of the cell cycle, to design more potent anticancer drugs. © 2012 IUBMB IUBMB Life, 64(7): 636–643, 2012

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“…Several preclinical and clinical trials have shown that nonsteroidal anti-inflammatory drugs (NSAIDs), used as classical COX inhibitors, could reduce the incidence of cancers (Cha et al, 2007;Kang et al, 2005;Lin et al, 2005). Although the exact anticancer mechanisms of NSAIDs are not fully understood, it seems to be related closely to their suppression of COX enzyme and subsequent reduction in prostaglandin production (Kismet et al, 2004;Zatelli et al, 2005).…”

Section: The Influence Of Indomethacin On Abcg2 Expression and Functionmentioning

confidence: 99%

MCF-7 Breast Cancer Cell Line, a Model for the Study of the Association Between Inflammation and ABCG2-Mediated Multi Drug Resistance

Kalalinia¹,

Mosaffa²,

Behravan³

2011

Breast Cancer - Focusing Tumor Microenvironment, Stem Cells and Metastasis

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Combination of cyclooxygenase-2 inhibitors and oxaliplatin increases the growth inhibition and death in human colon cancer cells

Cited by 69 publications

References 40 publications

Comparison of oxaliplatin‐ and curcumin‐mediated antiproliferative effects in colorectal cell lines

Comparison of oxaliplatin‐ and curcumin‐mediated antiproliferative effects in colorectal cell lines

NSAIDs induce apoptosis in nonproliferating ovarian cancer cells and inhibit tumor growth in vivo

MCF-7 Breast Cancer Cell Line, a Model for the Study of the Association Between Inflammation and ABCG2-Mediated Multi Drug Resistance

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