Targeting lipid metabolism of cancer cells: A promising therapeutic strategy for cancer DOI Creative Commons

Qiuping Liu,

Qing Luo, Alexander Halim

et al.

Cancer Letters, Journal Year: 2017, Volume and Issue: 401, P. 39 - 45

Published: May 17, 2017

Language: Английский

PPARγ signaling and metabolism: the good, the bad and the future DOI
Maryam Ahmadian, Jae Myoung Suh, Nasun Hah

et al.

Nature Medicine, Journal Year: 2013, Volume and Issue: 19(5), P. 557 - 566

Published: May 1, 2013

Language: Английский

Citations

1692

Cancer Cachexia: Mediators, Signaling, and Metabolic Pathways DOI Creative Commons

Kenneth C.H. Fearon,

David J. Glass, Denis C. Guttridge

et al.

Cell Metabolism, Journal Year: 2012, Volume and Issue: 16(2), P. 153 - 166

Published: July 17, 2012

Language: Английский

Citations

1091

Adipose tissue browning and metabolic health DOI
Alexander Bartelt, Jöerg Heeren

Nature Reviews Endocrinology, Journal Year: 2013, Volume and Issue: 10(1), P. 24 - 36

Published: Oct. 22, 2013

Language: Английский

Citations

1044

Cell-intrinsic lysosomal lipolysis is essential for alternative activation of macrophages DOI
Stanley Ching‐Cheng Huang, Bart Everts,

Yulia Ivanova

et al.

Nature Immunology, Journal Year: 2014, Volume and Issue: 15(9), P. 846 - 855

Published: Aug. 3, 2014

Language: Английский

Citations

1033

PD-1 alters T-cell metabolic reprogramming by inhibiting glycolysis and promoting lipolysis and fatty acid oxidation DOI Creative Commons
Nikolaos Patsoukis, Kankana Bardhan, Pranam Chatterjee

et al.

Nature Communications, Journal Year: 2015, Volume and Issue: 6(1)

Published: March 26, 2015

During activation, T cells undergo metabolic reprogramming, which imprints distinct functional fates. We determined that on PD-1 ligation, activated are unable to engage in glycolysis or amino acid metabolism but have an increased rate of fatty β-oxidation (FAO). promotes FAO endogenous lipids by increasing expression CPT1A, and inducing lipolysis as indicated elevation the lipase ATGL, marker glycerol release acids. Conversely, CTLA-4 inhibits without augmenting FAO, suggesting sustains profile non-activated cells. Because utilize during differentiation effectors, our findings reveal a mechanism responsible for PD-1-mediated blockade T-effector cell differentiation. The enhancement provides mechanistic explanation longevity receiving signals patients with chronic infections cancer, their capacity be reinvigorated blockade.

Language: Английский

Citations

993

Fatty Acid Trafficking in Starved Cells: Regulation by Lipid Droplet Lipolysis, Autophagy, and Mitochondrial Fusion Dynamics DOI Creative Commons
Angelika S. Rambold, Sarah Cohen, Jennifer Lippincott‐Schwartz

et al.

Developmental Cell, Journal Year: 2015, Volume and Issue: 32(6), P. 678 - 692

Published: March 1, 2015

Language: Английский

Citations

853

Memory CD8+ T Cells Use Cell-Intrinsic Lipolysis to Support the Metabolic Programming Necessary for Development DOI Creative Commons
David O’Sullivan,

Gerritje J. W. van der Windt,

Stanley Ching‐Cheng Huang

et al.

Immunity, Journal Year: 2014, Volume and Issue: 41(1), P. 75 - 88

Published: July 1, 2014

Language: Английский

Citations

705

Emerging roles of lipid metabolism in cancer metastasis DOI Creative Commons
Xiangjian Luo,

Can Cheng,

Zheqiong Tan

et al.

Molecular Cancer, Journal Year: 2017, Volume and Issue: 16(1)

Published: April 11, 2017

Cancer cells frequently display fundamentally altered cellular metabolism, which provides the biochemical foundation and directly contributes to tumorigenicity malignancy. Rewiring of metabolic programmes, such as aerobic glycolysis increased glutamine are crucial for cancer shed from a primary tumor, overcome nutrient energy deficit, eventually survive form metastases. However, role lipid metabolism that confers aggressive properties malignant cancers remains obscure. The present review is focused on key enzymes in associated with metastatic disease pathogenesis. We also address function an important membrane structure-lipid raft mediating tumor progression. enumerate integrate these recent findings into our current understanding reprogramming metastasis accompanied by new exciting therapeutic implications.

Language: Английский

Citations

556

Immobilization of lipases on hydrophobic supports: immobilization mechanism, advantages, problems, and solutions DOI
Rafael C. Rodrigues, José J. Virgen-Ortíz, José Cleiton Sousa dos Santos

et al.

Biotechnology Advances, Journal Year: 2019, Volume and Issue: 37(5), P. 746 - 770

Published: April 8, 2019

Language: Английский

Citations

529

Novozym 435: the “perfect” lipase immobilized biocatalyst? DOI Creative Commons
Claudia Ortíz, Marı́a Luján Ferreira, Oveimar Barbosa

et al.

Catalysis Science & Technology, Journal Year: 2019, Volume and Issue: 9(10), P. 2380 - 2420

Published: Jan. 1, 2019

Novozym 435 (N435) is a commercially available immobilized lipase produced by Novozymes with its advantages and drawbacks.

Language: Английский

Citations

505