The Consumption of Omega-3 Polyunsaturated Fatty Acids Improves Clinical Outcomes and Prognosis in Pancreatic Cancer Patients: A Systematic Evaluation

Ma, Yingjie; Yu, Jing; Xiao, Jing; Cao, Bangwei

doi:10.1080/01635581.2015.976315

Cited by 43 publications

(32 citation statements)

References 29 publications

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“…Indeed, omega‐3 fatty acid supplements (i.e., DHA, EPA) have been reported to provide promising muscle‐sparing effects against disease‐associated cachexia and sarcopenia (Ma et al. ; Pappalardo et al. ; Smith et al.…”

Section: Discussionmentioning

confidence: 99%

Docosahexaenoic acid counteracts palmitate‐induced endoplasmic reticulum stress in C2C12 myotubes: Impact on muscle atrophy

et al. 2017

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Lipid accumulation in skeletal muscle results in dysregulation of protein metabolism and muscle atrophy. We previously reported that treating C2C12 myotubes with palmitate (PA), a saturated fatty acid, increases the overall rate of proteolysis via activation of the ubiquitin‐proteasome and autophagy systems; co‐treatment with the omega‐3 polyunsaturated fatty acid docosahexaenoic acid (DHA) prevents the PA‐induced responses. Others have reported that PA induces endoplasmic reticulum (ER) stress which initiates the unfolded protein response (UPR), a collective group of responses that can lead to activation of caspase‐mediated proteolysis and autophagy. Presently, we tested the hypothesis that DHA protects against PA‐induced ER stress/UPR and its atrophy‐related responses in muscle cells. C2C12 myotubes were treated with 500 μmol/L PA and/or 100 μmol/L DHA for 24 h. Proteins and mRNA associated with ER stress/UPR, autophagy, and caspase‐3 activation were evaluated. PA robustly increased the phosphorylation of protein kinase R (PKR)‐like ER kinase (PERK) and eukaryotic initiation factor 2α (eIF2α). It also increased the mRNAs encoding activating transcription factor 4 (ATF4), spliced X‐box binding protein 1 (XBP1s), C/EBP homologous protein (CHOP), and autophagy‐related 5 (Atg5) as well as the protein levels of the PERK target nuclear factor erythroid 2‐related factor (Nrf2), CHOP, and cleaved (i.e., activated) caspase‐3. Co‐treatment with DHA prevented all of the PA‐induced responses. Our results indicate that DHA prevents PA‐induced muscle cell atrophy, in part, by preventing ER stress/UPR, a process that leads to activation of caspase‐mediated proteolysis and an increase in expression of autophagy‐related genes.

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Section: Discussionmentioning

confidence: 99%

Docosahexaenoic acid counteracts palmitate‐induced endoplasmic reticulum stress in C2C12 myotubes: Impact on muscle atrophy

et al. 2017

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“…Total dietary fat consumption was reported to be independently associated with pancreatic cancer risk according to one meta-analysis (33), although this has been refuted (8). Results regarding the association between omega-3 polyunsaturated fatty acid consumption and pancreatic cancer risk/survival are mixed (34,35).…”

Section: Metabolic Syndrome and Pancreatic Cancer Riskmentioning

confidence: 98%

Statins and pancreatic cancer

et al. 2017

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Abstract. Pancreatic cancer remains among the most lethal cancers, despite ongoing advances in treatment for all stages of the disease. Disease prevention represents another opportunity to improve patient outcome, with metabolic syndrome and its components, such as diabetes, obesity and dyslipidemia, having been recognized as modifiable risk factors for pancreatic cancer. In addition, statins have been shown to potentially reduce pancreatic cancer risk and to improve survival in patients with a combination of metabolic syndrome and pancreatic cancer. Furthermore, preclinical studies have demonstrated that statins exhibit antitumor effects in pancreatic cancer cell lines in vitro and animal models in vivo, in addition to delaying the progression of pancreatic intraepithelial neoplasia to pancreatic ductal adenocarcinoma (PDAC) and inhibiting PDAC formation in conditional K-Ras mutant mice. The mechanisms by which statins produce anticancer effects remain poorly understood, although appear to involve inhibition of the mevalonate/cholesterol synthesis pathway, thus blocking the synthesis of intermediates important for prenylation and activation of the Ras/mitogen-activated protein kinase 1 signaling pathway. Furthermore, statins have been identified to modulate the phosphoinositide 3-kinase/Akt serine/threonine kinase 1 and inflammation signaling pathways, and to alter the expression of genes involved in lipid metabolism, which are important for PDAC growth and proliferation. In addition, statins have been demonstrated to exhibit further antitumor mechanisms in a number of other cancer types, which are beyond the scope of the present review. In the present review, current evidence highlighting the potential of statins as chemopreventive agents in pancreatic cancer is presented, and the antitumor mechanisms of statins elucidated thus far in this disease are discussed.

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“…Encouraging results concerning the in vivo anti-neoplastic activity of n- 3 PUFAs have been also obtained from clinical studies, even though they were mainly set-up to investigate cancer prevention and support, rather than cancer therapy [ 25 , 30 , 31 , 90 , 91 , 92 , 93 , 94 , 95 , 96 , 97 , 98 , 99 , 100 , 101 ]. Indeed, the outcomes mainly investigated included n- 3 PUFAs membrane incorporation, immune and inflammatory responses, oxidative status, as well as body weight and composition or quality of life [ 31 , 96 , 97 , 99 , 100 , 101 ].…”

Section: Induction Of Cancer Cell Apoptosis By N- mentioning

confidence: 99%

Omega-3 Fatty Acids and Cancer Cell Cytotoxicity: Implications for Multi-Targeted Cancer Therapy

D'Eliseo

Velotti

2016

JCM

243

185

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Cancer is a major disease worldwide. Despite progress in cancer therapy, conventional cytotoxic therapies lead to unsatisfactory long-term survival, mainly related to development of drug resistance by tumor cells and toxicity towards normal cells. n-3 polyunsaturated fatty acids (PUFAs), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), can exert anti-neoplastic activity by inducing apoptotic cell death in human cancer cells either alone or in combination with conventional therapies. Indeed, n-3 PUFAs potentially increase the sensitivity of tumor cells to conventional therapies, possibly improving their efficacy especially against cancers resistant to treatment. Moreover, in contrast to traditional therapies, n-3 PUFAs appear to cause selective cytotoxicity towards cancer cells with little or no toxicity on normal cells. This review focuses on studies investigating the cytotoxic activity of n-3 PUFAs against cancer cells via apoptosis, analyzing the molecular mechanisms underlying this effective and selective activity. Here, we highlight the multiple molecules potentially targeted by n-3 PUFAs to trigger cancer cell apoptosis. This analysis can allow a better comprehension of the potential cytotoxic therapeutic role of n-3 PUFAs against cancer, providing specific information and support to design future pre-clinical and clinical studies for a better use of n-3 PUFAs in cancer therapy, mainly combinational therapy.

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The Consumption of Omega-3 Polyunsaturated Fatty Acids Improves Clinical Outcomes and Prognosis in Pancreatic Cancer Patients: A Systematic Evaluation

Cited by 43 publications

References 29 publications

Docosahexaenoic acid counteracts palmitate‐induced endoplasmic reticulum stress in C2C12 myotubes: Impact on muscle atrophy

Docosahexaenoic acid counteracts palmitate‐induced endoplasmic reticulum stress in C2C12 myotubes: Impact on muscle atrophy

Statins and pancreatic cancer

Omega-3 Fatty Acids and Cancer Cell Cytotoxicity: Implications for Multi-Targeted Cancer Therapy

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