Four types of fatty acids exert differential impact on pancreatic cancer growth

Yu, Ming; Liu, Hongyi; Duan, Yijie; Zhang, David; Li, Shasha; Wang, Feng

doi:10.1016/j.canlet.2015.02.002

Cited by 38 publications

(41 citation statements)

References 23 publications

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“…The role of fatty acids in pancreatic cancer, however, remains poorly understood. Fatty acids were found to alter the proliferation of pancreatic cancer cells in vitro , and n-6 polyunsaturated fatty acids were shown to promote the liver metastasis of a xenograft tumor model in vivo [33]. In the present study, we found that culture of cancer cells in adipose tissue conditioned medium increased the number of lipid droplets per cell, accompanied by increased invasiveness, reduced proliferation and enhanced chemoresistance in vitro .…”

Section: Discussionsupporting

confidence: 57%

Extra-pancreatic invasion induces lipolytic and fibrotic changes in the adipose microenvironment, with released fatty acids enhancing the invasiveness of pancreatic cancer cells

et al. 2017

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Pancreatic cancer progression involves components of the tumor microenvironment, including stellate cells, immune cells, endothelial cells, and the extracellular matrix. Although peripancreatic fat is the main stromal component involved in extra-pancreatic invasion, its roles in local invasion and metastasis of pancreatic cancer remain unclear. This study investigated the role of adipose tissue in pancreatic cancer progression using genetically engineered mice (Pdx1-Cre; LSL-KrasG12D; Trp53R172H/+) and an in vitro model of organotypic fat invasion. Mice fed a high fat diet had significantly larger primary pancreatic tumors and a significantly higher rate of distant organ metastasis than mice fed a standard diet. In the organotypic fat invasion model, pancreatic cancer cell clusters were smaller and more elongated in shape and showed increased fibrosis. Adipose tissue-derived conditioned medium enhanced pancreatic cancer cell invasiveness and gemcitabine resistance, as well as inducing morphologic changes in cancer cells and increasing the numbers of lipid droplets in their cytoplasm. The concentrations of oleic, palmitoleic, and linoleic acids were higher in adipose tissue-derived conditioned medium than in normal medium, with these fatty acids significantly enhancing the migration of cancer cells. Mature adipocytes were smaller and the concentration of fatty acids in the medium higher when these cells were co-cultured with cancer cells. These findings indicate that lipolytic and fibrotic changes in peripancreatic adipose tissue enhance local invasiveness and metastasis via adipocyte-released fatty acids. Inhibition of fatty acid uptake by cancer cells may be a novel therapy targeting interactions between cancer and stromal cells.

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Section: Discussionsupporting

confidence: 57%

Extra-pancreatic invasion induces lipolytic and fibrotic changes in the adipose microenvironment, with released fatty acids enhancing the invasiveness of pancreatic cancer cells

et al. 2017

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“…The former are generally associated with protective effects against colon cancer, while the latter have adverse effects [20–23]. The ω3 PUFAs can reduce cancer cell growth and differentiation by suppressing AA and the downstream eicosanoid biosynthesis [24, 25].…”

Section: Lipids In Crcmentioning

confidence: 99%

Lipidome in colorectal cancer

Yan

Zhu

et al. 2016

Oncotarget

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Colorectal cancer (CRC) is the second leading cause of cancer-related deaths. Understanding its pathophysiology is essential for developing efficient strategies to treat this disease. Lipidome, the sum of total lipids, related enzymes, receptors and signaling pathways, plays crucial roles in multiple cellular processes, such as metabolism, energy storage, proliferation and apoptosis. Dysregulation of lipid metabolism and function contributes to the development of CRC, and can be used towards the evaluation of prognosis. The strategies targeting lipidome have been applied in clinical trails and showed promising results. Here we discuss recent advances in abnormal lipid metabolism in CRC, the mechanisms by which the lipidome regulates tumorigenesis and tumor progression, and suggest potential therapeutic targets for clinical trials.

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“…When rodents were treated with pancreatic carcinogens or were genetically prone to pancreatic cancer, the genesis and growth of pancreatic cancer cells were stimulated by SFA-, MUFA-, and n6PUFA-enriched diets and inhibited by n3PUFA-enriched diet [7][8][9][10][11][12][13][14]. When mature human pancreatic cancer cells were transplanted in the pancreas of athymic mice, they were stimulated by SFA-, MUFA-, and n6PUFA-enriched diets and inhibited by n3PUFA-enriched diet [15,16]. In vitro, the growth of pancreatic cancer cells was increased by SFA and MUFA, inhibited by n3PUFA, and diversified in the presence of n6PUFA [16][17][18][19].…”

Section: Habitual Intake Of High Fat Diet (Hfd)mentioning

confidence: 99%

Increased dietary fatty acids determine the fatty-acid profiles of human pancreatic cancer cells and their carrier’s plasma, pancreas and liver

Qiu

Wang

et al. 2019

Endocr J

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Primary contents of dietary fat are three or four types of fatty acids, namely saturated fatty acid (SFA), monounsaturated fatty acid (MUFA), n6-polyunsaturated fatty acid (n6PUFA) and, to less extent, n3-polyunsaturated fatty acid (n3PUFA). Previous studies suggest that increased SFA, MUFA, and n6PUFA in high fat diets (HFDs) stimulate the origination, growth, and liver metastasis of pancreatic cancer cells, whereas increased n3PUFA has the opposite effects. It is unclear whether the fatty acid-induced effects are based on changed fatty-acid composition of involved cells. Here, we investigated whether increased SFA, MUFA, n6PUFA, and n3PUFA in different HFDs determine the FA profiles of pancreatic cancer cells and their carrier's plasma, pancreas, and liver. We transplanted MiaPaCa2 human pancreatic cancer cells in athymic mice and fed them normal diet or four HFDs enriched with SFA, MUFA, n6PUFA, and n3PUFA, respectively. After 7 weeks, fatty acids were profiled in tumor, plasma, pancreas, and liver, using gas chromatography. When tumor carriers were fed four HFDs, the fatty acids that were increased dietarily were also increased in the plasma. When tumor carriers were fed MUFA-, n6PUFA-, and n3PUFA-enriched HFDs, the dietarily increased fatty acids were also increased in tumor, pancreas, and liver. When tumor-carriers were fed the SFA-enriched HFD featuring lauric and myristic acids (C12:0 and C14:0), tumor, pancreas, and liver showed an increase not in the same SFAs but palmitic acid (C16:0) and/or stearic acid (C18:0). In conclusion, predominant fatty acids in HFDs determine the fatty-acid profiles of pancreatic cancer cells and their murine carriers.

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Four types of fatty acids exert differential impact on pancreatic cancer growth

Cited by 38 publications

References 23 publications

Extra-pancreatic invasion induces lipolytic and fibrotic changes in the adipose microenvironment, with released fatty acids enhancing the invasiveness of pancreatic cancer cells

Extra-pancreatic invasion induces lipolytic and fibrotic changes in the adipose microenvironment, with released fatty acids enhancing the invasiveness of pancreatic cancer cells

Lipidome in colorectal cancer

Increased dietary fatty acids determine the fatty-acid profiles of human pancreatic cancer cells and their carrier’s plasma, pancreas and liver

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