Leuktriene synthesis by human gastrointestinal tissues

Dreyling, K. W.; Hoppe, U.; Peskar, Bernhard A.; Morgenroth, K; Kozuschek, W.; Peskar, B. M.

doi:10.1016/0005-2760(86)90145-1

Cited by 79 publications

(28 citation statements)

References 21 publications

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“…In addition, previous reports provide evidence supporting a possible role for LTA 4 H and LTB 4 in cancer cell progression. Notably, higher expression of LTA 4 H (17) and an elevated production level of LTB 4 (31) in colon cancer tissue have been reported. In addition, LTB 4 was reported to stimulate the proliferation of colorectal cancer cells (32).…”

Section: Discussionmentioning

confidence: 99%

[6]-Gingerol Suppresses Colon Cancer Growth by Targeting Leukotriene A4 Hydrolase

et al. 2009

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Abstract[6]-Gingerol, a natural component of ginger, exhibits antiinflammatory and antitumorigenic activities. Despite its potential efficacy in cancer, the mechanism by which [6]-gingerol exerts its chemopreventive effects remains elusive. The leukotriene A 4 hydrolase (LTA 4 H) protein is regarded as a relevant target for cancer therapy. Our in silico prediction using a reverse-docking approach revealed that LTA 4 H might be a potential target of

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Section: Discussionmentioning

confidence: 99%

[6]-Gingerol Suppresses Colon Cancer Growth by Targeting Leukotriene A4 Hydrolase

et al. 2009

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“…Since the major metabolite in the 5-LOX pathway is LTB 4 , the involvement of LTB 4 in carcinogenesis in various organs has also been indicated (16,17). In addition, overproduction of LTB 4 in human colon cancer tissue and rat esophageal adenocarcinomas (18,19) and LTB 4 -mediated proliferation of colon cancer cells were reported (20,21). Thus, many fragmentary studies indicate the critical role of the LTB 4 -signaling pathway on the proliferation of colon cancer cells, but stronger evidences, such as direct proof of LTB 4 -receptor expression in colon cancer tissue and knockdown of the LTB 4 receptor itself by the siRNA approach, are required for definitive proof.…”

Section: Discussionmentioning

confidence: 99%

Blockade of Leukotriene B4 Signaling Pathway Induces Apoptosis and Suppresses Cell Proliferation in Colon Cancer

et al. 2007

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Abstract. We investigated whether leukotriene B 4 (LTB 4 ) and its signaling pathway play an important role in the progression of human colon cancer via a direct stimulation of cancer cell proliferation. Remarkable expression of LTB 4 receptor 1 (BLT1) in human colon cancer tissues was detected by immunohistochemistry, and Western blot analysis revealed the BLT1 expression in cultured human colon cancer cell lines, Caco2 and HT29. The 5-lipoxygenase inhibitor AA-861 and LTB 4 -receptor antagonist U75302 showed negative effects on survival and proliferation of both Caco2 and HT-29 cells. The inhibition of cell proliferation is due to the apoptosis because nuclear condensation and increased annexin V expression were observed in the cells treated with AA-861 and U75302. Knockdown of BLT1 by small interfering RNA caused the suppression of BLT1 protein, resulting in the inhibition of cancer cell proliferation. Blockade of BLT1 by the receptor antagonist significantly suppresses the LTB 4 -stimulated extracellular signal-regulated kinase (ERK) activation in colon cancer cells. These results indicate that the blockade of the LTB 4 -signaling pathway induces apoptosis via the inhibition of ERK activation in colon cancer cells. The LTB 4 -signaling pathway might be a new therapeutic target for colon cancer.

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“…The human colon is also able to produce lipoxygenase metabolites [16] and these AA-derived metabolites have also been implicated in the control of intestinal epithelial cell growth. Thus, endogenous production of LTD 4 mediates autocrine survival and proliferation via the nuclear-and membrane-located CysLT 1 receptor, triggering a proliferative ERK1/2 signal in non-transformed and transformed intestinal epithelial cells [15,35].…”

Section: Role Of Eicosanoids In the Control Of Intestinal Epithelial mentioning

confidence: 99%

“…Shoji et al [12] Transformed and non-transformed intestinal epithelial cell lines [13][14][15] as well as the human intestine [16,17] also produce LOX metabolites such as LTs and HETEs, whereas there is no information about HETE/EET production by cytochrome P-450 in intestinal epithelial cells or the intestine. With respect to the presence of LT receptors in the intestine, the CysLT 1 receptor is expressed in intestinal epithelial cells and tumorderived intestinal cells [15] whereas the CysLT 2 receptor is expressed in differentiated intestinal epithelial cells but not in tumor-derived intestinal cell lines [18].…”

mentioning

confidence: 99%

Role of eicosanoids on intestinal epithelial homeostasis

Ferrer

Moreno

2010

Biochemical Pharmacology

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The intestinal epithelium is a highly dynamic system that is continuously renewed by a process involving cell proliferation and differentiation. Moreover, it is the main interface with the external environment, and maintenance and regulation of the epithelial structure and epithelial barrier function are key determinants of digestive health and host well-being. The tight junction, a multiprotein complex composed of transmembrane proteins associated with the cytoskeletal peri-junctional ring of actin and myosin, is an essential component of this barrier that is strictly regulated in a spatio-temporal manner by a complex signaling network. Defects in the intestinal epithelial barrier function have been observed in inflammatory bowel disease, and a classic example of the connection between inflammation and cancer is the increased risk of colorectal cancer in patients with inflammatory bowel disease. In recent years, several molecules have emerged as critical players contributing to inflammationassociated colorectal cancer. For example, eicosanoids derived from arachidonic acid are proposed as mediators involved in the regulation of epithelial structure/function. Interestingly, the tissue concentration of eicosanoids increases during mucosal inflammation and colorectal cancer development. This overview focuses on the physiological and physiopathological roles of eicosanoids in cell growth/cell differentiation/apoptosis and in the paracellular permeability of the intestinal epithelium. A better understanding of these processes will foster new ideas for the development of therapies for these chronic disorders.

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Leuktriene synthesis by human gastrointestinal tissues

Cited by 79 publications

References 21 publications

[6]-Gingerol Suppresses Colon Cancer Growth by Targeting Leukotriene A4 Hydrolase

[6]-Gingerol Suppresses Colon Cancer Growth by Targeting Leukotriene A4 Hydrolase

Blockade of Leukotriene B4 Signaling Pathway Induces Apoptosis and Suppresses Cell Proliferation in Colon Cancer

Role of eicosanoids on intestinal epithelial homeostasis

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