NSAIDs and Cell Proliferation in Colorectal Cancer

Ettarh, Raj; Cullen, Anthony; Calamai, Alvise

doi:10.3390/ph3072007

Cited by 20 publications

(16 citation statements)

References 63 publications

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“…Other non-opiate therapies that have been shown to reduce CIBP and disease progression in preclinical models of bone cancer are NSAIDS and inhibitors of COX-2 3,11,21,22,45,48 . Both these therapies have also been shown to slow the growth of a wide variety of cancers and are commonly used as a first line therapy to treat CIBP 3,11,21,22,45,48 .…”

Section: Discussionmentioning

confidence: 99%

“…Both these therapies have also been shown to slow the growth of a wide variety of cancers and are commonly used as a first line therapy to treat CIBP 3,11,21,22,45,48 . Additionally, at least in preclinical models, anti-NGF therapy has also been shown to reduce the growth of head and neck cancer as well as reducing tumor-induced bone remodeling and time to fracture in a mouse model of bone cancer pain 30,52,79,97 .…”

Section: Discussionmentioning

confidence: 99%

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Targeting cells of the myeloid lineage attenuates pain and disease progression in a prostate model of bone cancer

Thompson

Jiménez-Andrade

Chartier

et al. 2015

Pain

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Targeting cells of the myeloid lineage attenuates pain and disease progression in a prostate model of bone cancer

Thompson

Jiménez-Andrade

Chartier

et al. 2015

Pain

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“…28) As described in the Introduction part, a number of indole compounds have been shown to induce cell death such as apoptosis by numerous mechanisms. 4,5) Thus, the effects of MW-03 on cellular growth were evaluated in LS174T cells treated with 0.1 to 10 µM of MW-03 for 48 h. As shown in Fig.…”

Section: Effects Of Mw-03 On Pge 2 -Induced Camp Formationmentioning

confidence: 99%

Anti-cancer Effects of MW-03, a Novel Indole Compound, by Inducing 15-Hydroxyprostaglandin Dehydrogenase and Cellular Growth Inhibition in the LS174T Human Colon Cancer Cell Line

Seira

Yanagisawa

Suganami

et al. 2017

Biological & Pharmaceutical Bulletin

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Increases in the expression of prostaglandin E 2 (PGE 2 ) are widely known to be involved in aberrant growth in the early stage of colon cancer development. We herein demonstrated that the novel indole compound MW-03 reduced PGE 2 -induced cAMP formation by catalization to an inactive metabolite by inducing 15-hydroxyprostaglandin dehydrogenase through the activation of peroxisome proliferator-activated receptor-γ. MW-03 also inhibited colon cancer cell growth by arresting the cell cycle at the S phase. Although the target of MW-03 for cell cycle inhibition has not yet been identified, these dual anti-cancer effects of MW-03 itself and/or its leading compound(s) on colon cancer cells may reduce colon cancer development and, thus, have potential as a novel treatment for the early stage of this disease.Key words indole compound; MW-03; prostaglandin E 2 ; 15-hydroxyprostaglandin dehydrogenase; peroxisome proliferator-activated receptor-γ; colon cancer One major prostanoid, prostaglandin E 2 (PGE 2 ) is widely known to be up-regulated by the action of increased levels of cyclooxygenase-2 (COX-2) in colorectal cancer.1,2) Thus, the enhanced expression of COX-2 and biosynthesis of PGE 2 are responsible for the malignancy of diseases.1,2) Since the overexpression of COX-2 and PGE 2 is frequently observed in the early stage of colorectal cancer development, they are considered to be the biomarkers of this stage. 3)Cruciferous vegetables, such as cauliflower, cabbage, and broccoli, are regarded as good food sources for reducing the risk of cancer including colon cancer. 4,5) Natural compounds that contain indole structures are relatively rich in cruciferous vegetables. 4,5) The consumption of cruciferous vegetables has been recommended by the National Research Council in the United States because of the protective mechanisms of phytochemicals including derivatives of indoles, e.g. indole-3-carbinol and diindolylmethane.4,5) These indole derivatives have been shown to induce cancer cell death such as apoptosis; although many mechanisms are suggested and reported, 4,5) the exact mechanisms underlying currently remain unclear. These cell death mechanisms are not only exerted by phytochemical indoles, but also by synthesized indoles such as one popular non-steroidal anti-inflammatory drug (NSAID), indomethacin. 6,7)Some indole compounds have been used as tools for researching prostanoid receptors and/or their signaling pathways. Among them, indomethacin has been used as an E-type prostanoid 2 (EP2) prostanoid receptor antagonist, 8) D-type prostanoid receptor antagonist, 9,10) chemoattractant receptorhomologous molecule expressed on T helper 2 cell receptor agonist, 11) and peroxisome proliferator-activated receptor-γ (PPARγ) agonist/antagonist, 12,13) by itself and/or its leading compounds with cyclooxygenase inhibition-independent activities.14) A previous study reported that indomethacin induced 15-hydroxyprostaglandin dehydrogenase (15-PGDH), an enzyme that catalyzes prostanoids such as PGE 2 to inactive, the metabolite...

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“…Increased levels of mPGES-1 have been found in various cancers, including non-small-cell lung cancer, colon cancer, and prostate cancer [Larsson et al, 2015]. Animal studies have shown that chemical inhibition or the elimination of COX-2 activity results in a decreased or slower tumor formation [Jänne and Mayer, 2000;Ettarh et al, 2010]. Sulforaphane (SFN) is a member of the isothiocyanate family present in cruciferous vegetables such as broccoli and broccoli sprouts [Dashwood and Ho, 2008;Ho et al, 2009].…”

Section: Introductionmentioning

confidence: 99%

Sulforaphane, a Chemopreventive Compound, Inhibits Cyclooxygenase-2 and Microsomal Prostaglandin E Synthase-1 Expression in Human HT-29 Colon Cancer Cells

Tafakh

Saidijam

Ranjbarnejad

et al. 2018

Cells Tissues Organs

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Background: A high expression of prostaglandin E2 (PGE2) is found in colorectal cancer. Therefore, blocking of PGE2 generation has been identified as a promising approach for anticancer therapy. Sulforaphane (SFN), an isothiocyanate derived from glucosinolate, is used as the antioxidant and anticancer agents. Methods: HT-29 cells were treated with various concentrations of SFN and compared to untreated cells for the expression of microsomal prostaglandin E synthase-1 (mPGES-1), cyclooxygenase 2 (COX-2), hypoxia-inducible factor-1 (HIF-1), C-X-C chemokine receptor type 4 (CXCR4), vascular endothelial growth factor (VEGF), and matrix metalloproteinase (MMP)-2 and MMP-9 at the mRNA level. The PGE2 level was measured by ELISA assay. Apoptosis was evaluated by the proportion of sub-G1 cells. The activity of caspase-3 was determined using an enzymatic assay. HT-29 cell migration was assessed using a scratch test. Results: SFN preconditioning decreased the expression of COX-2, mPGES-1, HIF-1, VEGF, CXCR4, MMP-2, and MMP-9. An apoptotic effect of SFN was preceded by the activation of caspase-3 as well as accumulation of cells in the sub-G1 phase of the cell cycle. SFN decreased PGE2 generation and inhibited the in vitro motility/wound-healing activity of HT-29 cells. Conclusions: SFN anticancer effects are associated with antiproliferative, antiangiogenic, and antimetastatic activities arising from the downregulation of the COX-2/ mPGES-1 axis.

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NSAIDs and Cell Proliferation in Colorectal Cancer

Cited by 20 publications

References 63 publications

Targeting cells of the myeloid lineage attenuates pain and disease progression in a prostate model of bone cancer

Targeting cells of the myeloid lineage attenuates pain and disease progression in a prostate model of bone cancer

Anti-cancer Effects of MW-03, a Novel Indole Compound, by Inducing 15-Hydroxyprostaglandin Dehydrogenase and Cellular Growth Inhibition in the LS174T Human Colon Cancer Cell Line

Sulforaphane, a Chemopreventive Compound, Inhibits Cyclooxygenase-2 and Microsomal Prostaglandin E Synthase-1 Expression in Human HT-29 Colon Cancer Cells

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