Prostate cancer vs hyperplasia: relationships with prostatic and adipose tissue fatty acid composition

Mamalakis, George; Kafatos, A.; Kalogeropoulos, Nick; Andrikopoulos, Nikolaos K.; Daskalopulos, G.; Kranidis, Athanasios

doi:10.1054/plef.2002.0384

Cited by 59 publications

(44 citation statements)

References 69 publications

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“…The level of AA then diminished over time suggesting metabolism of the AA into PGE2 (Hughes-Fulford et al, 2005) or HETEs. This potential rapid metabolism of AA, correlating with patient data (Mamalakis et al, 2002;Faas et al, 2003), suggests that AA cyclooxgenase and lipoxygenase products are potentially important components of the cancer process.…”

Section: Discussionmentioning

confidence: 79%

“…The study by (Mamalakis et al, 2002) also showed that despite a reduction of AA in prostatic tissues between CaP and BPH patients there was no significant difference in the levels of AA within the adipose tissue. We therefore hypothesised that the level of AA within the adipocyte-rich BMS may be maintained in CaP patients and act as an attractant for metastatic PEC.…”

Section: Discussionmentioning

confidence: 92%

“…in the prostate cancer patients (Mamalakis et al, 2002), we sought to determine the rate of lipid uptake. PC-3 cells cultured in the presence of 10 mM AA and stained with Nile Red rapidly took up the PUFA from the local environment (within 15 min), reaching a maximum level of uptake after 45 min.…”

Section: Discussionmentioning

confidence: 99%

“…Mamalakis et al (2002) showed that relative to benign disease patients, the adipose tissue and prostatic tissue of CaP patients had reduced levels of AA and the o-3 lipid docosahexaenoic acid (DHA), and a reduced o-3 : o-6 PUFA ratio. Adipocyte/epithelial cell interactions have been shown to induce proliferation of prostate (Tokuda et al, 2003) and mammary (Rahimi et al, 1994) cancer cell lines and plays an important role in normal breast development (Zangani et al, 1999).…”

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confidence: 99%

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Promotion of prostatic metastatic migration towards human bone marrow stoma by Omega 6 and its inhibition by Omega 3 PUFAs

et al. 2006

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Epidemiological studies have shown not only a relationship between the intake of dietary lipids and an increased risk of developing metastatic prostate cancer, but also the type of lipid intake that influences the risk of metastatic prostate cancer. The Omega-6 polyunsaturated fatty acid, Arachidonic acid, has been shown to enhance the proliferation of malignant prostate epithelial cells and increase the risk of advanced prostate cancer. However, its role in potentiating the migration of cancer cells is unknown. Here we show that arachidonic acid at concentrations p5 mM is a potent stimulator of malignant epithelial cellular invasion, which is able to restore invasion toward hydrocortisone-deprived adipocyte-free human bone marrow stroma completely. This observed invasion is mediated by the arachidonic acid metabolite prostaglandin E 2 and is inhibited by the Omega-3 poly-unsaturated fatty acids eicosapentaenoic acid and docosahexaenoic acid at a ratio of 1 : 2 Omega-3 : Omega-6, and by the COX-2 inhibitor NS-398. These results identify a mechanism by which arachidonic acid may potentiate the risk of metastatic migration and secondary implantation in vivo, a risk which can be reduced with the uptake of Omega-3 poly-unsaturated fatty acids.

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Section: Discussionmentioning

confidence: 79%

Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Promotion of prostatic metastatic migration towards human bone marrow stoma by Omega 6 and its inhibition by Omega 3 PUFAs

et al. 2006

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“…A marked difference in the composition of fatty acids and the gene expression profile between prostate cancer and BPH cells or tissues has been described. 29,30 This implies the disassociation of the Ser447stop polymorphism with risk of BPH, while the Ser447stop polymorphism is specifically involved in the development of prostate cancer by affecting fatty acid metabolism.…”

Section: Discussionmentioning

confidence: 99%

Association of lipoprotein lipase gene polymorphism with risk of prostate cancer in a japanese population

Narita

Tsuchiya

Wang

et al. 2004

Intl Journal of Cancer

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Prostate cancer has a prominent variation in incidence among different racial/ethnic groups. Previous studies have demonstrated that nutritional factors, especially fat intake, may contribute to the development and progression of prostate cancer. In fact, animal studies have shown that lower fat intake inhibits prostate cancer growth. 1,2 Giovannucci et al. 3 have demonstrated a marked increase in the likelihood of prostate cancer in men with a high fat intake from red meat and a significant association between the total intake of essential fatty acids such as ␣-linolenic acid and the development of aggressive prostate cancer. On the other hand, the significance of genetic factors in the development and progression of prostate cancer has been well documented. While the incidence of prostate cancer in the native Japanese population is 5 times lower than that in Caucasians, Japanese Americans have an approximately 40 -50% higher rate of prostate cancer than Japanese men, but the rate of prostate cancer in Japanese American men does not appear to approach that of Caucasians. 4,5 These reports further support the concept that genetic factors in combination with dietary factors may have a significant impact on susceptibility to prostate cancer. In exploring genetic susceptibility factors for prostate cancer, a population whose nutritional or environmental factors are small may be an ideal cohort, in which individual differences in such factors and gene-environment interactions are minimized. It has been reported that the calorie intake and the proportion of fat to total calories consumed are quite low in Japan compared to those in Western countries. 6 Therefore, the Japanese might be an ideal population to investigate the association between polymorphisms and prostate cancer risk because the nutritional factors may be minimized.Lipoprotein lipase (LPL) plays a crucial role in fat metabolism. LPL hydrolyses triglycerides in both chylomicrons and very-lowdensity lipoproteins (VLDLs) and liberates free fatty acids. The human LPL gene is localized to chromosome 8p22. The gene contains 10 exons and has several DNA variants designated as Ser447stop, HindIII and PvuII polymorphisms. These polymorphisms have been shown to underlie changes in plasma lipoprotein levels and to be one of the important risk factors for cardiovascular diseases. 7-9 However, no information is available on the relationship between these LPL polymorphisms and prostate cancer risk.In this study, with the hypothesis that the LPL polymorphisms may be associated with the onset and/or progression of prostate cancer, we analyzed the LPL genotype of patients with prostate cancer or benign prostatic hyperplasia (BPH) as compared with male controls in a native Japanese population. MATERIAL AND METHODS SubjectsA total of 708 subjects consisting of 273 prostate cancer patients, 205 BPH patients and 230 male controls who visited Akita University Medical Center, its related community hospitals and Kyoto University Hospital were enrolled in this study. Because thi...

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Effect of glucose and palmitate environment on proliferation and migration of PC3‐prostate cancer cells

Rezende

Galheigo

Landim

et al. 2019

Cell Biology International

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Recent studies have been trying to find out how diet and metabolic changes such as dyslipidaemia, hyperglycaemia, and hyperinsulinaemia can stimulate cancer progression. This investigation aimed to evaluate the effect of high concentrations of fatty acids and/or glucose in tumour prostate cells, focusing on the proliferation/migration profile and oxidative stress. PC3 cells were treated with high concentration of saturated fatty acid (palmitate, 100 mM), glucose (220 mg/dL), or both for 24 or 48 h. Results demonstrated that PC3 cells showed a significant increase in proliferation after 48 h of treatment with glucose and palmitateþglucose. Cell proliferation was associated with reduced levels of AMPK phosphorylation in glucose group at 24 and 48 h of treatment, while palmitate group presented this result only after 48 h of treatment. Also, there was a significant increase in cell migration between time 0 and 48 h after all treatments, except in the control. Catalase activity was increased by palmitate in the beginning of treatment, while glucose presented a later effect. Also, nitrite production was increased by glucose only after 48 h, and the total antioxidant activity was enhanced by palmitate in the initial hours. Thus, we conclude that the high concentration of the saturated fatty acid palmitate and glucose in vitro influences PC3 cells and stimulates cellular activities related to carcinogenesis such as cell proliferation, migration, and oxidative stress in different ways. Palmitate presents a rapid and initial effect, while a glucose environment stimulates cells later on, maintaining high levels of cell proliferation.

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Prostate cancer vs hyperplasia: relationships with prostatic and adipose tissue fatty acid composition

Cited by 59 publications

References 69 publications

Promotion of prostatic metastatic migration towards human bone marrow stoma by Omega 6 and its inhibition by Omega 3 PUFAs

Promotion of prostatic metastatic migration towards human bone marrow stoma by Omega 6 and its inhibition by Omega 3 PUFAs

Association of lipoprotein lipase gene polymorphism with risk of prostate cancer in a japanese population

Effect of glucose and palmitate environment on proliferation and migration of PC3‐prostate cancer cells

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