The implications of signaling lipids in cancer metastasis

Luo, Xiangjian; Zhao, Xu; Cheng, Chunxia; Li, Namei; Liu, Ying; Cao, Yang

doi:10.1038/s12276-018-0150-x

Cited by 79 publications

(64 citation statements)

References 114 publications

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“…Indeed, there is increasing literature linking lipid metabolism to cancer, 43,44 to migration and invasion, 45 but also to metastasis. 46 Bertini et al found in a study of serum metabolic profiles that altered lipid levels were associated with reduced survival of synchronously metastasized CRC patients. 16 In breast cancer, altered membrane lipid metabolism had been reported to underlie disease progression.…”

Section: Discussionmentioning

confidence: 99%

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Non‐invasive metastasis prognosis from plasma metabolites in stage II colorectal cancer patients: The DACHS study

Zaimenko

Jaeger

Brenner

et al. 2019

Intl Journal of Cancer

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Metastasis is the main cause of death from colorectal cancer (CRC). About 20% of stage II CRC patients develop metastasis during the course of disease. We performed metabolic profiling of plasma samples from non‐metastasized and metachronously metastasized stage II CRC patients to assess the potential of plasma metabolites to serve as biomarkers for stratification of stage II CRC patients according to metastasis risk. We compared the metabolic profiles of plasma samples prospectively obtained prior to metastasis formation from non‐metastasized vs. metachronously metastasized stage II CRC patients of the German population‐based case–control multicenter DACHS study retrospectively. Plasma samples were analyzed from stage II CRC patients for whom follow‐up data including the information on metachronous metastasis were available. To identify metabolites distinguishing non‐metastasized from metachronously metastasized stage II CRC patients robust supervised classifications using decision trees and support vector machines were performed and verified by 10‐fold cross‐validation, by nested cross‐validation and by traditional validation using training and test sets. We found that metabolic profiles distinguish non‐metastasized from metachronously metastasized stage II CRC patients. Classification models from decision trees and support vector machines with 10‐fold cross‐validation gave average accuracy of 0.75 (sensitivity 0.79, specificity 0.7) and 0.82 (sensitivity 0.85, specificity 0.77), respectively, correctly predicting metachronous metastasis in stage II CRC patients. Taken together, plasma metabolic profiles distinguished non‐metastasized and metachronously metastasized stage II CRC patients. The classification models consisting of few metabolites stratify non‐invasively stage II CRC patients according to their risk for metachronous metastasis.

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Section: Discussionmentioning

confidence: 99%

“…Metabolites involved in lipid and linoleic metabolism constituted a major part of identified metabolic signature distinguishing NON from MET patients. Indeed, there is increasing literature linking lipid metabolism to cancer, to migration and invasion, but also to metastasis …”

Section: Discussionmentioning

confidence: 99%

Non‐invasive metastasis prognosis from plasma metabolites in stage II colorectal cancer patients: The DACHS study

Zaimenko

Jaeger

Brenner

et al. 2019

Intl Journal of Cancer

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“…Reprogramming energy metabolism represents one of the hallmarks of cancer cells . As a core regulator of mitochondrial biogenesis and metabolism, the emerging roles of PGC‐1α implicated in tumorgenesis and progression have been gradually unraveled.…”

Section: Discussionmentioning

confidence: 99%

Posttranslational regulation of PGC‐1α and its implication in cancer metabolism

Luo

Liao

Quan

et al. 2019

Intl Journal of Cancer

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Deregulation of cellular metabolism is well established in cancer. The mitochondria are dynamic organelles and act as the center stage for energy metabolism. Central to mitochondrial regulatory network is peroxisome proliferator‐activated receptor γ coactivator 1a (PGC‐1α), which serves as a master regulator of mitochondrial proliferation and metabolism. The activity and stability of PGC‐1α are subject to dynamic and versatile posttranslational modifications including phosphorylation, ubiquitination, methylation and acetylation in response to metabolic stress and other environmental signals. In this review, we describe the structure of PGC‐1α. Then, we discuss recent advances in the posttranslational regulatory machinery of PGC‐1α, which affects its transcriptional activity, stability and organelle localization. Furthermore, we address the important roles of PGC‐1α in tumorigenesis and malignancy. Finally, we also mention the clinical therapeutic potentials of PGC‐1α modulators. A better understanding of the elegant function of PGC‐1α in cancer progression could provide novel insights into therapeutic interventions through the targeting of PGC‐1α signaling.

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“…In this way, melanoma cells metabolism was considerably affected and melanoma progression sustained by increased uptake of FAs from TME-resident adipocytes, hence revisiting FATPs as new possible targets in melanoma therapy (56). Moreover, beyond cell energetic requirements, lipid alterations can also affect lipid signaling in melanoma (57,58). Indeed, FAs can bind and activate specific nuclear receptors, i.e., PPARs, thus controlling the expression of genes involved in lipid homeostasis, oxidative stress, and inflammation (59,60).…”

Section: Metabolic Pathways In Melanomamentioning

confidence: 99%

The Complex Role of Autophagy in Melanoma Evolution: New Perspectives From Mouse Models

2020

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Despite tremendous efforts in the last decade to improve treatments, melanoma still represents a major therapeutic challenge and overall survival of patients remains poor. Therefore, identifying new targets to counteract melanoma is needed. In this scenario, autophagy, the "self-eating" process of the cell, has recently arisen as new potential candidate in melanoma. Alongside its role as a recycling mechanism for dysfunctional and damaged cell components, autophagy also clearly sits at a crossroad with metabolism, thereby orchestrating cell proliferation, bioenergetics and metabolic rewiring, all hallmarks of cancer cells. In this regard, autophagy, both in tumor and host, has been flagged as an essential player in melanomagenesis and progression. To pave the way to a better understanding of such a complex interplay, the use of genetically engineered mouse models (GEMMs), as well as syngeneic mouse models, has been undoubtedly crucial. Herein, we will explore the latest discoveries in the field, with particular focus on the potential of these models in unraveling the contribution of autophagy in melanoma, along with the therapeutic advantages that may arise.

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The implications of signaling lipids in cancer metastasis

Cited by 79 publications

References 114 publications

Non‐invasive metastasis prognosis from plasma metabolites in stage II colorectal cancer patients: The DACHS study

Non‐invasive metastasis prognosis from plasma metabolites in stage II colorectal cancer patients: The DACHS study

Posttranslational regulation of PGC‐1α and its implication in cancer metabolism

The Complex Role of Autophagy in Melanoma Evolution: New Perspectives From Mouse Models

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