Lipoprotein lipase in non-small cell lung cancer tissue is highly expressed in a subpopulation of tumor-associated macrophages

Podgornik, Helena; Sok, Mihael; Kern, Izidor; Marc, Janja; Černe, Darko

doi:10.1016/j.prp.2013.06.004

Cited by 19 publications

(12 citation statements)

References 23 publications

(40 reference statements)

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“…The FAs released by hydrolysis of circulating TGs can be taken up by the cells via CD36, a transmembrane channel protein for exogenous free FA uptake. High LPL activity was reported in non-small cell lung cancer tissue [37]. LPL has also been identified as a biomarker for poor prognosis in chronic lymphocytic leukemia [38].…”

Section: Lipid Metabolism In the Tumor Microenvironmentmentioning

confidence: 99%

Lipid metabolism and lipophagy in cancer

Maan

Peters

Dutta

et al. 2018

Biochemical and Biophysical Research Communications

195

151

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The tumor microenvironment can be hypoxic, acidic, and deficient in nutrients, thus causing the metabolism of tumor cells as well as the neighboring stromal cells to be remodelled to facilitate tumor survival, proliferation, and metastasis. Abnormal tumor lipid metabolism is a fairly new field, which has received attention in the past few years. Cross-talk between tumor cells and tumor-associated stromal cells modulates the high metabolic needs of the tumor. Fatty acid turnover is high in tumor cells to meet the energy as well as synthetic requirements of the growing tumor. Lipolysis of lipids stored in lipid droplets was earlier considered to be solely carried out by cytosolic lipases. However recent studies demonstrate that lipophagy (autophagic degradation of lipids by acidic lipases) serves as an alternate pathway for the degradation of lipid droplets. Involvement of lipophagy in lipid turnover makes it a crucial player in tumorigenesis and metastasis. In this review we discuss the metabolic reprogramming of tumor cells with special focus on lipid metabolism. We also address the lipid turnover machinery in the tumor cell, especially the lipophagic pathway. Finally, we integrate the current understanding of lipophagy with tumor lipid metabolism.

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Section: Lipid Metabolism In the Tumor Microenvironmentmentioning

confidence: 99%

Lipid metabolism and lipophagy in cancer

Maan

Peters

Dutta

et al. 2018

Biochemical and Biophysical Research Communications

195

151

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“…Interestingly, the increased LPL activity in cancer tissue, compared with healthy lung tissue, predicts lower overall survival in non-small-cell lung cancer [ 20 , 21 ]. The location of tumor LPL is somewhat controversial as a recent study observed that increased LPL expression was in a subgroup of macrophages and not in cancer cells [ 69 ]. These studies mostly report gene expression and therefore future studies linking functional changes in cancer cell LPL activity driving FA release from circulating TAG are required, especially as LPL activity is regulated by a variety of physiological stimuli (see review [ 70 ]).…”

Section: Lipoprotein Hydrolysis Fatty Acid Transport and Trafficmentioning

confidence: 99%

Obesity and Cancer Progression: Is There a Role of Fatty Acid Metabolism?

Balaban

Lee

Schreuder

et al. 2015

BioMed Research International

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Currently, there is renewed interest in elucidating the metabolic characteristics of cancer and how these characteristics may be exploited as therapeutic targets. Much attention has centered on glucose, glutamine and de novo lipogenesis, yet the metabolism of fatty acids that arise from extracellular, as well as intracellular, stores as triacylglycerol has received much less attention. This review focuses on the key pathways of fatty acid metabolism, including uptake, esterification, lipolysis, and mitochondrial oxidation, and how the regulators of these pathways are altered in cancer. Additionally, we discuss the potential link that fatty acid metabolism may serve between obesity and changes in cancer progression.

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“…All LGI3-regulated and NSCLC-altered genes were found in the previous literature on NSCLC that reported an association of genetic variations, expression and function of these genes with NSCLC. Expression levels of PTGS2 (26), IL6 (27), CCL2 (28), NCF1/2 (29), CXCL2 (30), CSF3 (31), CXCL13 (32), LPL (33), SERPINE1 (34), PPARG (35) and FABP4 (36), and the promoter methylation of DLK1 (37) have been reported to be associated with the prognosis and pathogenesis of NSCLC. A total of seven genes (PTGS2, IL6, CCL2, NCF2, CXCL2, CSF3 and NCF1) that have been reported to be increased by LGI3 may be downregulated in NSCLC due to the suppression of LGI3 expression.…”

Section: Discussionmentioning

confidence: 99%

Leucine rich repeat LGI family member 3: Integrative analyses reveal its prognostic association with non‑small cell lung cancer

2019

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Leucine rich repeat LGI family member 3 (LGI3) is a member of the LGI protein family. Our previous studies reported that LGI3 was expressed in adipose tissues, brain and skin, where it served roles as a multifunctional cytokine and pro-inflammatory adipokine. It was hypothesized that LGI3 may be involved in cytokine networks in cancer. The present study aimed to analyze differentially expressed genes in non-small cell lung cancer (NSCLC) tissues and NSCLC cohort data, to evaluate the prognostic role of LGI3. Expression microarray and NSCLC cohort data were statistically analyzed by bioinformatic methods, and protein-protein interactions, functional enrichment and pathway, gene coexpression network (GCN) and prognostic association analyses were performed. The results demonstrated that the expression levels of LGI3 and its receptor a disintegrin and metalloproteinase domain-containing protein 22 were significantly decreased in NSCLC tissues. A total of two upregulated genes and 11 downregulated genes in NSCLC tissues were identified as LGI3-regulated genes. Protein-protein interaction network analysis demonstrated that all LGI3-regulated genes that were altered in NSCLC were involved in a protein-protein interaction network cluster. Functional enrichment, Kyoto Encyclopedia of Genes and Genomes pathway and GCN analyses demonstrated the association of these genes with the immune and inflammatory responses, angiogenesis, the tumor necrosis factor pathway, and chemokine and peroxisome proliferator-activated receptor signaling pathways. Analysis of NSCLC cohorts revealed that low expression levels of LGI3 was significantly associated with poor prognosis of NSCLC. Analysis of the somatic mutations of the LGI3 gene in NSCLC revealed that the amino acid residues altered in NSCLC included two single nucleotide polymorphism sites and three phylogenetically coevolved amino acid residues. Taken together, these results suggest that LGI3 may be a potential prognostic marker of NSCLC.

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Lipoprotein lipase in non-small cell lung cancer tissue is highly expressed in a subpopulation of tumor-associated macrophages

Cited by 19 publications

References 23 publications

Lipid metabolism and lipophagy in cancer

Lipid metabolism and lipophagy in cancer

Obesity and Cancer Progression: Is There a Role of Fatty Acid Metabolism?

Leucine rich repeat LGI family member 3: Integrative analyses reveal its prognostic association with non‑small cell lung cancer

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