Fish oil prevents colon cancer by modulation of structure and function of mitochondria

Agnihotri, Navneet; Sharma, Geeta; Rani, Isha; Renuka, .; Bhatnagar, Archana

doi:10.1016/j.biopha.2016.04.045

Cited by 19 publications

(16 citation statements)

References 55 publications

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“…Transmission electron microscopy (TEM) imaging was performed as previous described [ 42 ]. The mouse colon specimens were embedded in epoxy resin and cut into ultrathin sections (60–70 nm).…”

Section: Methodsmentioning

confidence: 99%

MiR-155 contributes to intestinal barrier dysfunction in DSS-induced mice colitis via targeting HIF-1α/TFF-3 axis

Liu

Zhu

et al. 2020

Aging

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Intestinal barrier dysfunction is a hallmark of inflammatory bowel disease (IBD). MiR-155 is increased in colitis and downregulates expression of hypoxia-inducible factor 1α (HIF-1α). Here, we investigated the effects of miR-155 on intestinal barrier dysfunction in dextran sulfate sodium (DSS)-induced colitis. We found that miR-155 antagomir treatment relieved weight loss and intestinal damage in IBD mouse models (P < 0.05). Furthermore, electron microscopy and immunofluorescence imaging showed that miR-155 increased intestinal barrier dysfunction and downregulated the expression of tight junction proteins in DSS-induced colitis. FG-4497, which upregulates HIF-1α expression, elicited protective effects on the intestinal barrier in DSS-induced colitis. Dual luciferase reporter assays also confirmed that miR-155 downregulated expression of HIF-1α. Finally, we discovered that HIF-1α levels were elevated by miR-155 antagomir treatment (P < 0.05) and that TFF-3 expression correlated positively with HIF-1α expression. These results suggest that miR-155 contributes to DSS-induced colitis by promoting intestinal barrier dysfunction and inhibiting the HIF-1α/TFF-3 axis.

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Section: Methodsmentioning

confidence: 99%

MiR-155 contributes to intestinal barrier dysfunction in DSS-induced mice colitis via targeting HIF-1α/TFF-3 axis

Liu

Zhu

et al. 2020

Aging

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“…-Primary tumour growth and resistance to treatment- In a recent study focusing on colorectal carcinogenesis, male Wistar rats received a weekly intraperitoneal injections of ethylenediamine tetra-acetic acid (EDTA) or N,Ndimethylhydrazine dihydrochloride (DMH) for a period of 4 weeks, responsible for the initiation and post-initiation phase, respectively (285). These groups were subdivided into dietary groups, a control group, a group receiving fish oil and corn oil in similar proportions…”

Section: The Perspectives Of Using Dietary Lipids For An Integrated Smentioning

confidence: 99%

“…Interestingly, fish oil diet in both the ratios stabilized or increased the number of mitochondria. The diet the more enriched in fish oil induced mitophagy, along with modulation of the electron transport chain complexes activity, decreased cholesterol and cardiolipin (a specific phospholipid of mitochondrial membranes containing four acyl chains) levels, thus facilitating apoptosis and attenuating carcinogenesis(285).In PC3 prostate cancer cells, treating the cells with fish oil, containing 90% ethyl ester n-3 fatty acid among which 40% DHA, 40% EPA, and 10% other n-3 PUFA, induced important phosphoproteomic changes as compared to a control group treated with oleic acid.Particularly relevant are the phosphorylation levels of the two regulatory serine residues in pyruvate dehydrogenase alpha 1 (PDHA1), serine-232 and serine-300, which were significantly decreased upon fish oil treatment, resulting in the increase of pyruvate dehydrogenase (PDH) activity. Results brought by this study supported the protective role of n-3 PUFA in prostate cancer through the suppression of aerobic glycolysis by restoring PDH activity, and in controlling the balance between lipid and glucose oxidation(286).Metabolic investigation were also performed in breast cancer cells showing respiratory (BT-474 cell line) or glycolytic (MDA-MB-231 cell line) phenotypes, compared to non-cancerMCF-10 mammary cells, and revealed that DHA supplementation significantly diminished the cancer cell metabolism and glycolytic profile of malignant cell lines in a dosedependent manner (287).…”

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confidence: 99%

Metabolic reprogramming in cancer cells, consequences on pH and tumour progression: Integrated therapeutic perspectives with dietary lipids as adjuvant to anticancer treatment

Dumas

Brisson

Chevalier

et al. 2017

Seminars in Cancer Biology

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While tumours arise from acquired mutations in oncogenes or tumour-suppressor genes, it is clearly established that cancers are metabolic diseases characterized by metabolic alterations in tumour cells, and also non-tumour cells of the host organism resulting in tumour cachexia and patient weakness. In this review, we aimed at delineating details by which metabolic alterations in cancer cells, characterized by mitochondrial bioenergetics deregulations and the preference for aerobic glycolysis, are critical parameters controlling the aggressive progression of tumours. In particular, metabolic alteration in cancer cells are coupled to the modulation of intracellular and extracellular pH, epithelial-to-mesenchymal transition and associated increased invasiveness, autophagy, and the development of anticancer treatment resistance. Finally, based on mechanistic, pre-clinical and clinical studies, we proposed the adjuvant supplementation of dietary n-3 polyunsaturated fatty acids for a complementary holistic treatment of the cancer disease.

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“…Результаты проспективного исследования типа «случай-контроль» (European Prospective Investigation into Cancer and Nutrition, EPIC, 2014) показали, что концентрации ХС ЛПВП и аполипопротеина A1 отрицательно связаны с риском развития рака толстой кишки [20]. Напротив, по данным N. Agnihotri и соавт., увеличение потребление общего жира, холестерина, насыщенных жиров и красного мяса тесно связано с развитием КРР [21].…”

Section: Discussionunclassified

Study of the Level of Fatty Acids in Erythrocyte Membranes and Serum of Patients With Colorectal Cancer in Novosibirsk

et al. 2018

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The objectiveis to measure the level of fatty acids in erythrocyte membranes and serum of patients with colorectal cancer.Materials and methods.The study group included 100 patients with diagnosed colorectal cancer (57 men and 43 women). The control group included 24 reasonably healthy people (14 men and 10 women) matched for age and sex, without malignant cancers or manifested pathology of the internal organs.Results.Decreased levels of saturated, monounsaturated fatty acids and increased levels of polyunsaturated fatty acids (PUFAs) in erythrocyte membranes and serum (p <0.0001–0.05) were observed. The levels of omega-3 PUFAs in colorectal cancer exceeded the levels in healthy individuals both in erythrocyte membranes and in serum; for omega-6 PUFAs only a trend was observed. At the same time, the ratio of omega-6/omega-3 PUFAs in colorectal cancer was lower than in control (p <0.0001–0.002). The state of erythrocyte membranes more significantly and for more parameters characterized differences between the groups than serum. The most discriminating parameters between patients with colorectal cancer and healthy individuals both in erythrocyte membranes and serum were the levels of C20:2;11,14 (eicosadienoic), C20:3;8,11,14 (dihomo-γ-linolenic), C20:4;5,8,11,14 (eicosatetraenoic, arachidonic), C22:5;7,10,13,16,19 (docosapentaenoic), and C22:6;4,7,10,13,16,19 (docosahexaenoic) PUFAs.

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Fish oil prevents colon cancer by modulation of structure and function of mitochondria

Cited by 19 publications

References 55 publications

MiR-155 contributes to intestinal barrier dysfunction in DSS-induced mice colitis via targeting HIF-1α/TFF-3 axis

MiR-155 contributes to intestinal barrier dysfunction in DSS-induced mice colitis via targeting HIF-1α/TFF-3 axis

Metabolic reprogramming in cancer cells, consequences on pH and tumour progression: Integrated therapeutic perspectives with dietary lipids as adjuvant to anticancer treatment

Study of the Level of Fatty Acids in Erythrocyte Membranes and Serum of Patients With Colorectal Cancer in Novosibirsk

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