Effects of eicosatrienoic acid (20:3 n-9, Mead’s acid) on some promalignant-related properties of three human cancer cell lines

Heyd, V.L; Eynard, A.R.

doi:10.1016/s1098-8823(03)00037-6

Cited by 20 publications

(23 citation statements)

References 26 publications

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“…In these two experiments, the mechanism of growth suppression was decreased cell proliferation, not accelerated apoptosis. Studies of the effects of MA on breast cancer in humans and animals are limited (14)(15)(16). MA dose-dependently inhibits vascular endothelial growth factor (VEGF)-stimulated angiogenesis (28).…”

Section: Discussionmentioning

confidence: 99%

“…Epidemiologically, MA was inversely associated with breast cancer risk as well as overall cancer risk (14). Experimentally, MA suppressed MCF-7 and KPL-1 human breast cancer cell growth in culture (15,16). MCF-7 and KPL-1 are luminal A Dietary effects of mead acid on N-methyl-N-nitrosoureainduced mammary cancers in female Sprague-Dawley rats subtypes according to intrinsic subtype classification (17).…”

Section: Introductionmentioning

confidence: 99%

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Dietary effects of mead acid on N-methyl-N-nitrosourea-induced mammary cancers in female Sprague-Dawley rats

et al. 2015

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Abstract. The effect of mead acid (MA;5,8, on the suppression of the development and growth of N-methyl-N-nitrosourea (MNU)-induced mammary cancer in female Sprague-Dawley rats was examined. The MA diet (2.4% MA) or control (CTR) diet (0% MA) was started at 6 weeks of age, MNU was injected intraperitoneally at 7 weeks of age, and the rats were maintained on the respective diets for the whole experimental period (until 19 weeks of age). All induced mammary tumors were luminal A subtype carcinomas (estrogen and progesterone receptor positive and HER2/neu negative). The MA diet significantly suppressed the initiation and promotion phases of mammary carcinogenesis; MA suppressed the development (incidence, 61.5 vs. 100%; multiplicity, 2.1 vs. 4.5) and the growth (final tumor weight, 427.1 vs. 1,796.3 mg) of mammary cancers by suppressing cell proliferation, but not by accelerating cell death. There were evident changes in the major fatty acid composition of n-3, n-6, and n-9 fatty acids in the serum of the MA diet group; there was a significant increase in MA and significant decreases in oleic acid (OA), linoleic acid, arachidonic acid and docosahexaenoic acid. In non-tumorous mammary tissue, there was a significant increase in MA and a significant decrease in OA in the MA diet group. The n-6/n-3 ratios in serum and mammary tissue of the MA diet group were significantly decreased. The MA diet suppressed MNU-induced luminal A mammary cancer by lowering cancer cell proliferation. Therefore, MA may be a chemopreventive and chemotherapeutic agent. In addition to hormone therapy, MA supplementation may be a beneficial chemotherapeutic agent for the luminal A subtype of breast cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Dietary effects of mead acid on N-methyl-N-nitrosourea-induced mammary cancers in female Sprague-Dawley rats

et al. 2015

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“…Arachidonic acid (AA, 20:4n-6), docosahexaenoic acid (DHA, 22:6n-3), gamma-linolenic acid (GLA, 18:3n-6) and eicosapentaenoic acid (EPA, 20:5n-3) per se induced apoptosis of cancerous cells [6–9]. According to studies on glioma spheroids grown on collagen gels and on several glioma cell lines (C6, U373, U87 MG) GLA treatment was cytotoxic, while it did not influence normal cells [11].…”

Section: Introductionmentioning

confidence: 99%

Combination of unsaturated fatty acids and ionizing radiation on human glioma cells: cellular, biochemical and gene expression analysis

Antal

Hackler²,

Shen

et al. 2014

Lipids Health Dis

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BackgroundBased on previous observations a potential resort in the therapy of the particularly radioresistant glioma would be its treatment with unsaturated fatty acids (UFAs) combined with irradiation.MethodsWe evaluated the effect of different UFAs (arachidonic acid (AA), docosahexaenoic acid (DHA), gamma-linolenic acid (GLA), eicosapentaenoic acid (EPA) and oleic acid (OA)) on human U87 MG glioma cell line by classical biochemical end-point assays, impedance-based, real-time cellular and holographic microscopic analysis. We further analyzed AA, DHA, and GLA at morphological, gene and miRNA expression level.ResultsCorresponding to LDH-, MTS assays and real-time cytoxicity profiles AA, DHA, and GLA enhanced the radio sensitivity of glioma cells. The collective application of polyunsaturated fatty acids (PUFAs) and irradiation significantly changed the expression of EGR1, TNF-α, NOTCH1, c-MYC, TP53, HMOX1, AKR1C1, NQO1, while up-regulation of GADD45A, EGR1, GRP78, DDIT3, c-MYC, FOSL1 were recorded both in response to PUFA treatment or irradiation alone. Among the analyzed miRNAs miR-146 and miR-181a were induced by DHA treatment. Overexpression of miR-146 was also detected by combined treatment of GLA and irradiation.ConclusionsBecause PUFAs increased the radio responsiveness of glioma cells as assessed by biochemical and cellular assays, they might increase the therapeutic efficacy of radiation in treatment of gliomas. We demonstrated that treatment with DHA, AA and GLA as adjunct to irradiation up-regulated the expression of oxidative-stress and endoplasmic reticulum stress related genes, and affected NOTCH1 expression, which could explain their additive effects.Electronic supplementary materialThe online version of this article (doi:10.1186/1476-511X-13-142) contains supplementary material, which is available to authorized users.

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“…In the HRT-18 colon cancer cell line, ETA produced an increment in e-cadherin expression and lipid peroxidation but also increased proliferation. We concluded that this 18:1 derivative produced some procarcinogenic effects on three human cancer cell lines [141]. Other experiments in which ETA was added at a low concentration resulted in a reduction in the expression of e-cadherin, and to a lesser degree, of desmoglein, along with increased invasion of human squamous cell carcinoma (SCC) cells in vitro .…”

Section: Introductionmentioning

confidence: 99%

“…Other experiments in which ETA was added at a low concentration resulted in a reduction in the expression of e-cadherin, and to a lesser degree, of desmoglein, along with increased invasion of human squamous cell carcinoma (SCC) cells in vitro . At higher concentrations, ETA stimulated the growth of SCC cells [141, 142]. The promoting effects of OA and its metabolites on cancer cells were recently confirmed.…”

Section: Introductionmentioning

confidence: 99%

Basic aspects of tumor cell fatty acid-regulated signaling and transcription factors

Comba

Lin

Eynard

et al. 2011

Cancer Metastasis Rev

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This article reviews the current knowledge and experimental research about the mechanisms by which fatty acids and their derivatives control specific gene expression involved during carcinogenesis. Changes in dietary fatty acids, specifically the polyunsaturated fatty acids (PUFAs) of the ω-3 and ω-6 families and some derived eicosanoids from lipoxygenases (LOXs), cyclooxygenases (COXs), and cytochrome P-450 (CYP-450), seem to control the activity of transcription factor families involved in cancer cell proliferation or cell death. Their regulation may be carried out either through direct binding to DNA as peroxisome proliferator–activated receptors (PPARs) or via modulation in an indirect manner of signaling pathway molecules (e.g., protein kinase C [PKC]) and other transcription factors (nuclear factor kappa B [NFκB] and sterol regulatory element binding protein [SREBP]). Knowledge of the mechanisms by which fatty acids control specific gene expression may identify important risk factors for cancer, and provide insight into the development of new therapeutic strategies for a better management of whole-body lipid metabolism.

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Effects of eicosatrienoic acid (20:3 n-9, Mead’s acid) on some promalignant-related properties of three human cancer cell lines

Cited by 20 publications

References 26 publications

Dietary effects of mead acid on N-methyl-N-nitrosourea-induced mammary cancers in female Sprague-Dawley rats

Dietary effects of mead acid on N-methyl-N-nitrosourea-induced mammary cancers in female Sprague-Dawley rats

Combination of unsaturated fatty acids and ionizing radiation on human glioma cells: cellular, biochemical and gene expression analysis

Basic aspects of tumor cell fatty acid-regulated signaling and transcription factors

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