2006
DOI: 10.1016/j.jphotobiol.2006.02.003
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Pre-treatment of HT-29 cells with 5-LOX inhibitor (MK-886) induces changes in cell cycle and increases apoptosis after photodynamic therapy with hypericin

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Cited by 19 publications
(16 citation statements)
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“…COX-2 was found to be involved in the regulation of P-gp, MRP1 and BCRP transporter expression via the COX-2/PGE2̸PGE receptor 4̸phosphatidyl inositol 3-kinase pathway (116,118). Synergistic effects of NSAIDs with hypericin (HY)-mediated photodynamic therapy (PDT) have also been reported (119)(120)(121)(122). The specific inhibition of COX, LOX and CYP450 activity increased the efficacy of HY-PDT in the HT-29 cancer cell line (121).…”
Section: Combination Of Nsaids With Chemotherapeutic Drugs In Vitromentioning
confidence: 99%
“…COX-2 was found to be involved in the regulation of P-gp, MRP1 and BCRP transporter expression via the COX-2/PGE2̸PGE receptor 4̸phosphatidyl inositol 3-kinase pathway (116,118). Synergistic effects of NSAIDs with hypericin (HY)-mediated photodynamic therapy (PDT) have also been reported (119)(120)(121)(122). The specific inhibition of COX, LOX and CYP450 activity increased the efficacy of HY-PDT in the HT-29 cancer cell line (121).…”
Section: Combination Of Nsaids With Chemotherapeutic Drugs In Vitromentioning
confidence: 99%
“…MK-886 increased GluR1 phosphorylation in neuronal cultures in vitro and in the mouse cortex in vivo [Imbesi et al, 2007] and to inhibit the peroxisomeproliferator-activated receptor (PPAR)a [Kehrer et al, 2001]. MK-886 was thought to cause cell death in different cell types, such as enhancing N-acetylcysteine-induced apoptosis in Jurkat T lymphocytes [Deshpande and Kehrer., 2006], inducing changes in cell cycle and increased apoptosis after photodynamic therapy with hypericin in HT-29 cells [Kleban et al, 2006]; enhancing tumor necrosis factor-a-induced differentiation and apoptosis in HL-60 cells [Stika et al, 2006]; inducing apoptosis in gastric cancer through upregulation of p27kip1 and bax [Fan et al, 2004]; inducing apoptosis independently of 5-LO [Datta et al, 1999]; and activating voltage-gated and Ca…”
Section: Mk-886mentioning
confidence: 99%
“…In osteoblastic cells, Babich et al [1997] [Chang et al, 2005], 4,4 0 -dithiodipyridine [Kuo et al, 2003], CP55,940 [Lu et al, 2002b], and tamoxifen [Lu et al, 2002a]. Additionally, it appears that phospholipase C-dependent pathways did not play a role in MK-886-induced Ca MK-886 is cytotoxic in several cell types including Jurkat T lymphocytes [Deshpande and Kehrer., 2006], HT-29 cells [Kleban et al, 2006], HL-60 cells [Stika et al, 2006], gastric cancer cells [Fan et al, 2004], and rat arterial myocytes [Smirnov et al, 1998]. As lasting [Ca 21 ] i rises may lead to cell death [Annunziato et al, 2003], it is interesting to know whether MK-886-induced [Ca 21 ] i increases cause cell death in MG63 cells, given that [Ca 21 ] i rises are observed prior to MK-886-induced apoptosis in Bcl-2-positive U937 cells [Anderson et al, 2002[Anderson et al, , 2004.…”
Section: Involvement Of Apoptosis In Mk-886-induced Cell Deathmentioning
confidence: 99%
“…Among the characteristic constituents of H. perforatum are the naphthodianthrones, mainly represented by hypericin and pseudohypericin which have been the focus of extensive scientific research as important antiviral agents against a variety of viruses (herpes, murine cytomegalovirus, sindbis, hepatitis B, equine anemia, including the human immunodeficiency virus (HIV) [7]. Recently, H. perforatum naphthodianthrones have also been studied for their possible application in the photodynamic therapy of cancer [8]. The concentration of these constituents in the plant is particularly low, as mentioned above, varying from 0.01 to 0.03% and even in alcoholic or hydroalcoholic extracts it may reach up to 0.1 -0.4% [9].…”
Section: Introductionmentioning
confidence: 99%