Dietary lipids modulate eicosanoid release and apoptosis of cells of a murine lung alveolar carcinoma

Pasqualini, Marìa Eugenia; Berra, María Alejandra; Calderón, Reyna O.; Cremonezzi, David; Giraudo, C.; Eynard, Aldo R.

doi:10.1016/j.plefa.2004.11.002

Cited by 7 publications

(4 citation statements)

References 23 publications

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“…Feeding the mice a diet containing corn oil rich in n-6 PUFAs modulated the synthesis of eicosanoids (increasing 12-HETE and decreasing 12 HHT). These findings were positively correlated with an increment in apoptosis, diminution of mitosis and, concomitantly, with a decrease in tumoral growth [122]. Experimental studies on implanted C6 glioma cells into rat brains locally infused with 200 microM-2 mM of GLA have been shown the most active local concentration of GLA for antitumor activity was 2 mM, infused at 1 microl/h over 7 days.…”

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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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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“…The present study showed that BAX and Bcl-2 expression, markers of apoptosis and inhibition of apoptosis, respectively, were similar in FO and CO groups. Pasqualini et al (2005) found that neoplastic cells from the CO group showed a higher apoptosis count as compared with the olein group. High levels of arachidonic acid and decreased cyclooxygenase eicosanoids have been involved in antitumoral mechanisms by increasing tumor cell apoptosis.…”

Section: Discussionmentioning

confidence: 90%

“…Pasqualini et al. (2005) found that neoplastic cells from the CO group showed a higher apoptosis count as compared with the olein group.…”

Section: Discussionmentioning

confidence: 98%

Dietary Lipids Change the Expression of a Proliferation Marker in Murine 9,10‐dimethyl‐1,2‐benzanthracene‐induced Salivary Tumors

Actis

Cremonezzi

Lampe

et al. 2009

Journal of Food Lipids

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Salivary tumors were induced by 9,10‐dimethyl‐1,2‐benzanthracene injection into the submandibulary gland of mice fed with different dietary lipids. Tumor tissue from 10 mice fed with diets containing corn oil (CO) or fish oil (FO) were immunohistochemically stained for Cx26, β‐ and γ‐catenin, BAX, Bcl‐2 and Ki‐67. The percentage of animals showing different levels of biomarker expression in epithelial, mesenchymal and stromal cells was calculated in each group. The number of nuclei positive for Ki‐67 per 500 total cells was calculated. Reduced expression of Cx26 was observed in FO group as compared to CO. The staining was similar for β‐catenin, γ‐catenin, BAX and Bcl‐2 in both groups. The Ki‐67 labeling index was significantly different for CO and FO (0.45–0.40, P < 0.0008). The lower expression of Ki‐67 in FO mice could indicate less cellular proliferation. PRACTICAL APPLICATIONS Dietary fatty acids (FAs) affect tumorigenesis. This study examines the effect of dietary lipids on proliferation, apoptosis, cell adhesion and intercellular communication level change during tumorigenesis. Since dietary lipids may be protective or act as promoters of tumorigenesis, the beneficial and negative effects of different FAs could help inform nutrition recommendations directed to the population.

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“…Due to their intense activity at very low concentrations (even at values of nM or mM), it is easy to understand why there are no a pools of eicosanoids or BALs already formed in the body. Moreover, most eicosanoids arising from the same substrate (i.e., AA) exhibit an agonistic/antagonistic behavior, with their equilibrated balance being a key function as homeostatic cell controllers [37,38,58,59].…”

Section: Brief Reminder Of the Metabolism And Physiology Of Essential...mentioning

confidence: 99%

Crosstalk among dietary polyunsaturated fatty acids, urolithiasis, chronic inflammation, and urinary tract tumor risk

Eynard

Navarro

2013

Nutrition

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Dietary lipids modulate eicosanoid release and apoptosis of cells of a murine lung alveolar carcinoma

Cited by 7 publications

References 23 publications

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

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

Dietary Lipids Change the Expression of a Proliferation Marker in Murine 9,10‐dimethyl‐1,2‐benzanthracene‐induced Salivary Tumors

Crosstalk among dietary polyunsaturated fatty acids, urolithiasis, chronic inflammation, and urinary tract tumor risk

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