The diversity and breadth of cancer cell fatty acid metabolism

Nagarajan, Shilpa R.; Butler, Lisa M.; Hoy, Andrew J.

doi:10.1186/s40170-020-00237-2

Cited by 132 publications

(115 citation statements)

References 327 publications

(491 reference statements)

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“…Fasn activation promotes human cancer development, too, as was demonstrated in lung, pancreas, breast, ovarian, prostate, and colon cancers, which highlights the importance of lipogenesis in the development and progression of these tumors [35]. Inhibition of Fasn was shown to downregulate the β-catenin and mTOR signaling pathways [36], which is in good agreement with our findings.…”

Section: Alterations In Lipid Metabolismsupporting

confidence: 91%

Overexpression of Human Syndecan-1 Protects against the Diethylnitrosamine-Induced Hepatocarcinogenesis in Mice

Reszegi

Karászi

Tóth

et al. 2021

Cancers

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Although syndecan-1 (SDC1) is known to be dysregulated in various cancer types, its implication in tumorigenesis is poorly understood. Its effect may be detrimental or protective depending on the type of cancer. Our previous data suggest that SDC1 is protective against hepatocarcinogenesis. To further verify this notion, human SDC1 transgenic (hSDC1+/+) mice were generated that expressed hSDC1 specifically in the liver under the control of the albumin promoter. Hepatocarcinogenesis was induced by a single dose of diethylnitrosamine (DEN) at an age of 15 days after birth, which resulted in tumors without cirrhosis in wild-type and hSDC1+/+ mice. At the experimental endpoint, livers were examined macroscopically and histologically, as well as by immunohistochemistry, Western blot, receptor tyrosine kinase array, phosphoprotein array, and proteomic analysis. Liver-specific overexpression of hSDC1 resulted in an approximately six month delay in tumor formation via the promotion of SDC1 shedding, downregulation of lipid metabolism, inhibition of the mTOR and the β-catenin pathways, and activation of the Foxo1 and p53 transcription factors that lead to the upregulation of the cell cycle inhibitors p21 and p27. Furthermore, both of them are implicated in the regulation of intermediary metabolism. Proteomic analysis showed enhanced lipid metabolism, activation of motor proteins, and loss of mitochondrial electron transport proteins as promoters of cancer in wild-type tumors, inhibited in the hSDC1+/+ livers. These complex mechanisms mimic the characteristics of nonalcoholic steatohepatitis (NASH) induced human liver cancer successfully delayed by syndecan-1.

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Section: Alterations In Lipid Metabolismsupporting

confidence: 91%

Overexpression of Human Syndecan-1 Protects against the Diethylnitrosamine-Induced Hepatocarcinogenesis in Mice

Reszegi

Karászi

Tóth

et al. 2021

Cancers

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“…Cancer is a complex and heterogeneous disease that involves the dysregulation of various cell processes, such as metabolism ( 19 ), proliferation ( 20 ), intracellular pH dynamics ( 21 ), redox signaling ( 22 ), and migration/invasion ( 23 , 24 ). The complexity of this disease is also reflected by the different ecosystems that constitute a permissive TME ( 25 , 26 ).…”

Section: Immunological Tumor Microenvironmentmentioning

confidence: 99%

The Use of Iron Oxide Nanoparticles to Reprogram Macrophage Responses and the Immunological Tumor Microenvironment

2021

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The synthesis and functionalization of iron oxide nanoparticles (IONPs) is versatile, which has enhanced the interest in studying them as theranostic agents over recent years. As IONPs begin to be used for different biomedical applications, it is important to know how they affect the immune system and its different cell types, especially their interaction with the macrophages that are involved in their clearance. How immune cells respond to therapeutic interventions can condition the systemic and local tissue response, and hence, the final therapeutic outcome. Thus, it is fundamental to understand the effects that IONPs have on the immune response, especially in cancer immunotherapy. The biological effects of IONPs may be the result of intrinsic features of their iron oxide core, inducing reactive oxygen species (ROS) and modulating intracellular redox and iron metabolism. Alternatively, their effects are driven by the nanoparticle coating, for example, through cell membrane receptor engagement. Indeed, exploiting these properties of IONPs could lead to the development of innovative therapies. In this review, after a presentation of the elements that make up the tumor immunological microenvironment, we will review and discuss what is currently known about the immunomodulatory mechanisms triggered by IONPs, mainly focusing on macrophage polarization and reprogramming. Consequently, we will discuss the implications of these findings in the context of plausible therapeutic scenarios for cancer immunotherapy.

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“…In addition to their metabolic function, fatty acids play important roles as signalling molecules and in membrane structure. Cancer cells take advantage of two main fatty acid sources: de novo fatty acid synthesis, which is increased in several cancer cells including liver, prostate, colon and breast cancers [3], and the uptake from the surrounding extracellular microenvironment through transport proteins such as CD36 or Fatty Acid Binding Proteins (FAPBs) [4].…”

Section: Introductionmentioning

confidence: 99%

Adipocytes Promote Breast Cancer Cell Survival and Migration through Autophagy Activation

Bellanger

Dziagwa

Guimaraes

et al. 2021

Cancers

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White adipose tissue interacts closely with breast cancers through the secretion of soluble factors such as cytokines, growth factors or fatty acids. However, the molecular mechanisms of these interactions and their roles in cancer progression remain poorly understood. In this study, we investigated the role of fatty acids in the cooperation between adipocytes and breast cancer cells using a co-culture model. We report that adipocytes increase autophagy in breast cancer cells through the acidification of lysosomes, leading to cancer cell survival in nutrient-deprived conditions and to cancer cell migration. Mechanistically, the disturbance of membrane phospholipid composition with a decrease in arachidonic acid content is responsible for autophagy activation in breast cancer cells induced by adipocytes. Therefore, autophagy might be a central cellular mechanism of white adipose tissue interactions with cancer cells and thus participate in cancer progression.

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The diversity and breadth of cancer cell fatty acid metabolism

Cited by 132 publications

References 327 publications

Overexpression of Human Syndecan-1 Protects against the Diethylnitrosamine-Induced Hepatocarcinogenesis in Mice

Overexpression of Human Syndecan-1 Protects against the Diethylnitrosamine-Induced Hepatocarcinogenesis in Mice

The Use of Iron Oxide Nanoparticles to Reprogram Macrophage Responses and the Immunological Tumor Microenvironment

Adipocytes Promote Breast Cancer Cell Survival and Migration through Autophagy Activation

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