Eicosapentaenoic acid and docosahexaenoic acid inhibit macrophage-induced gastric cancer cell migration by attenuating the expression of matrix metalloproteinase 10

Wu, Ming-Hsun; Tsai, Yo‐Ting; Hua, Kuo Tai; Chang, Kun-Che; Mc, Kuo; Lin, Jaw–Town

doi:10.1016/j.jnutbio.2011.09.004

Cited by 34 publications

(23 citation statements)

References 65 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, MMP-10 was shown to promote invasive growth as silencing led to reduced transmigration of AGS in matrigel-coated chambers [51]. Similarly, MMP-10 from tumor associated macrophages was shown to increase AGS cell migration [87]. MMP-11 is also expressed in gastric cancer and expression levels increase with cancer progression.…”

Section: Deregulation Of Extracellular Host Proteases By H Pylorimentioning

confidence: 99%

Proteolysis in Helicobacter pylori-Induced Gastric Cancer

Posselt

Crabtree

Weßler

2017

Toxins

View full text Add to dashboard Cite

Persistent infections with the human pathogen and class-I carcinogen Helicobacter pylori (H. pylori) are closely associated with the development of acute and chronic gastritis, ulceration, gastric adenocarcinoma and lymphoma of the mucosa-associated lymphoid tissue (MALT) system. Disruption and depolarization of the epithelium is a hallmark of H. pylori-associated disorders and requires extensive modulation of epithelial cell surface structures. Hence, the complex network of controlled proteolysis which facilitates tissue homeostasis in healthy individuals is deregulated and crucially contributes to the induction and progression of gastric cancer through processing of extracellular matrix (ECM) proteins, cell surface receptors, membrane-bound cytokines, and lateral adhesion molecules. Here, we summarize the recent reports on mechanisms how H. pylori utilizes a variety of extracellular proteases, involving the proteases Hp0169 and high temperature requirement A (HtrA) of bacterial origin, and host matrix-metalloproteinases (MMPs), a disintegrin and metalloproteinases (ADAMs) and tissue inhibitors of metalloproteinases (TIMPs). H. pylori-regulated proteases represent predictive biomarkers and attractive targets for therapeutic interventions in gastric cancer.

show abstract

Section: Deregulation Of Extracellular Host Proteases By H Pylorimentioning

confidence: 99%

Proteolysis in Helicobacter pylori-Induced Gastric Cancer

Posselt

Crabtree

Weßler

2017

Toxins

View full text Add to dashboard Cite

show abstract

“… 26 Application of a diet enriched with n-3 PUFA delayed tumor growth in a mouse xenograft model. 27 In vitro studies have shown that n-3 PUFA inhibited macrophage-enhanced gastric cancer cell migration and attenuated matrix metalloproteinase (MMP)-10 expression through ERK and STAT3 phosphorylation 28 and inhibited the growth of human gastric carcinoma cell via apoptosis and combination with 5-fluorouracil has synergetic effect in inhibiting the proliferation of gastric cancer cells. 29 Moreover, n-3 PUFA are beneficial for preventing oxidative stress-induced apoptosis by inhibiting apoptotic gene expression and DNA fragmentation of gastric epithelial cells.…”

Section: The Efficacies Of N-3 Pufa In Prevention Of Gi Cancersmentioning

confidence: 99%

Omega-3 Polyunsaturated Fatty Acids as Potential Chemopreventive Agent for Gastrointestinal Cancer

Park¹,

Kwon²,

Han³

et al. 2013

J Cancer Prev

View full text Add to dashboard Cite

Omega-3 polyunsaturated fatty acids (n-3 PUFAs), particularly eicosapentanoic acid (EPA) and docosahexanoic acid (DHA), has been acknowledged as essential very long-chain fatty acids contributing to either achieving optimal health or protection against diseases, and even longevity. Recent high impact studies dealing with EPA and DHA have sparked a renewed interest in using n-3 PUFAs for cancer prevention and cancer treatment, for which n-3 PUFAs may exert their anticancer actions by influencing multiple targets implicated in various stages of cancer development, including cell proliferation, cell survival, angiogenesis, inflammation, and metastasis against various cancers. However, gastrointestinal cancers develop implicated with the close connection between inflammation and cancer and n-3 PUFAs especially imposed excellent actions of antiinflammation and antioxidation as well as their restorative actions. In detail, these beneficial lipids can restore or modify inflammation-associated lipid distorsion and alteration of lipid rafts. Although the chemopreventive effect of n-3 PUFAs has been studied in various experimental models, our understanding regarding the underlying mechanisms of n-3 PUFAs against GI cancer is still limited. In this review article, we described the in-detailed perspective and underlying mechanism of n-3 PUFAs application for GI cancers and added in vivo efficacy of n-3 PUFAs with Fat-1 transgenic mice experience. We suggest that future work should consider the n-6/n-3 FA ratio, combination treatment of other nutritions and alteration of lipid rafts to be a key element in experimental design and analysis.

show abstract

“…It also downregulated the MMP10 gene, which codes for a protein involved in cell-cell communication and metastasis. 14 Interestingly, a recent study has shown that eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) inhibit gastric cancer cell migration by suppressing the expression of matrix metalloproteinase 10. 14 Among the numerous genes altered by exposure of EpiOral tissues to antioxidants 1a, 1b, 2a, and 2b, only one gene was common in all four groups, ADRB2.…”

Section: Resultsmentioning

confidence: 99%

“…14 Interestingly, a recent study has shown that eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) inhibit gastric cancer cell migration by suppressing the expression of matrix metalloproteinase 10. 14 Among the numerous genes altered by exposure of EpiOral tissues to antioxidants 1a, 1b, 2a, and 2b, only one gene was common in all four groups, ADRB2. This gene encodes a β-2adrenergic receptor, which is a member of the G protein-coupled numerous essential roles in DNA damage response, cell cycle arrest, apoptosis, and transcription.…”

Section: Resultsmentioning

confidence: 99%

Novel antioxidants are not toxic to normal tissues but effectively kill cancer cells

Kovalchuk

Aladedunye

Rodriguez-Juarez

et al. 2013

Cancer Biology & Therapy

View full text Add to dashboard Cite

Free radicals are formed as a result of cellular processes and play a key role in predisposition to and development of numerous diseases and of premature aging. Recently, we reported the syntheses of a number of novel phenolic antioxidants for possible application in food industry. In the present study, analyses of the cellular processes and molecular gene expression effects of some of the novel antioxidants in normal human tissues and in cancer cells were undertaken. Results indicated that whereas the examined antioxidants showed no effects on morphology and gene expression of normal human oral and gingival epithelial tissues, they exerted a profound cell killing effect on breast cancer cells, including on chemotherapy-resistant breast cancer cells and on oral squamous carcinoma cells. Among the tested antioxidants, N-decyl-N-(3-methoxy-4-hydroxybenzyl)-3-(3,4-dihydroxyphenyl) propanamide and N-decyl-N-(3,5-dimethoxy-4-hydroxybenzyl)-3-(3,4-dihydroxyphenyl) propanamide were the most promising, with excellent potential for cancer treatment. Moreover, our gene expression databases can be used as a roadmap for future analysis of mechanisms of antioxidant action.

show abstract

Eicosapentaenoic acid and docosahexaenoic acid inhibit macrophage-induced gastric cancer cell migration by attenuating the expression of matrix metalloproteinase 10

Cited by 34 publications

References 65 publications

Proteolysis in Helicobacter pylori-Induced Gastric Cancer

Proteolysis in Helicobacter pylori-Induced Gastric Cancer

Omega-3 Polyunsaturated Fatty Acids as Potential Chemopreventive Agent for Gastrointestinal Cancer

Novel antioxidants are not toxic to normal tissues but effectively kill cancer cells

Contact Info

Product

Resources

About