Metabolic Plasticity of Melanoma Cells and Their Crosstalk With Tumor Microenvironment

Avagliano, Angelica; Fiume, Giuseppe; Pelagalli, Alessandra; Sanità, Gennaro; Ruocco, Maria Rosaria; Montagnani, Stefania; Arcucci, Alessandro

doi:10.3389/fonc.2020.00722

Cited by 77 publications

(101 citation statements)

References 242 publications

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“…The overabundance of pyruvic acid we observed among melanoma cells compared to EM is consistent with recent research that suggests it may accumulate in the cytosol as a result of sustained ERK1/2 activation in melanoma, leading to downregulation of pyruvate dehydrogenase and promotion of lactic fermentation—a hallmark of cancer [ 66 ].…”

Section: Discussionsupporting

confidence: 90%

Metabolomics of primary cutaneous melanoma and matched adjacent extratumoral microenvironment

et al. 2020

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Background Melanoma causes the vast majority of deaths attributable to skin cancer, largely due to its propensity for metastasis. To date, few studies have examined molecular changes between primary cutaneous melanoma and adjacent putatively normal skin. To broaden temporal inferences related to initiation of disease, we performed a metabolomics investigation of primary melanoma and matched extratumoral microenvironment (EM) tissues; and, to make inferences about progressive disease, we also compared unmatched metastatic melanoma tissues to EM tissues. Methods Ultra-high performance liquid chromatography—mass spectrometry-based metabolic profiling was performed on frozen human tissues. Results We observed 824 metabolites as differentially abundant among 33 matched tissue samples, and 1,118 metabolites as differentially abundant between metastatic melanoma (n = 46) and EM (n = 34) after false discovery rate (FDR) adjustment (p<0.01). No significant differences in metabolite abundances were noted comparing primary and metastatic melanoma tissues. Conclusions Overall, pathway-based results significantly distinguished melanoma tissues from EM in the metabolism of: ascorbate and aldarate, propanoate, tryptophan, histidine, and pyrimidine. Within pathways, the majority of individual metabolite abundances observed in comparisons of primary melanoma vs. EM and metastatic melanoma vs. EM were directionally consistent. This observed concordance suggests most identified compounds are implicated in the initiation or maintenance of melanoma.

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Section: Discussionsupporting

confidence: 90%

Metabolomics of primary cutaneous melanoma and matched adjacent extratumoral microenvironment

et al. 2020

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“…Furthermore, MYC is a pivotal player in the metabolic rewiring of cancer cells, the strategy that cancer cells adopt to cope with the energetic and metabolic demands required to support tumor growth and progression. [ 33 , 34 , 35 ]. MYC can contribute to tumorigenesis also influencing host immune cells [ 36 ].…”

Section: Myc and Lymphomagenesismentioning

confidence: 99%

Insights about MYC and Apoptosis in B-Lymphomagenesis: An Update from Murine Models

Vecchio

Fiume

Correnti

et al. 2020

IJMS

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The balance between cell survival and cell death represents an essential part of human tissue homeostasis, while altered apoptosis contributes to several pathologies and can affect the treatment efficacy. Impaired apoptosis is one of the main cancer hallmarks and some types of lymphomas harbor mutations that directly affect key regulators of cell death (such as BCL-2 family members). The development of novel techniques in the field of immunology and new animal models has greatly accelerated our understanding of oncogenic mechanisms in MYC-associated lymphomas. Mouse models are a powerful tool to reveal multiple genes implicated in the genesis of lymphoma and are extensively used to clarify the molecular mechanism of lymphoma, validating the gene function. Key features of MYC-induced apoptosis will be discussed here along with more recent studies on MYC direct and indirect interactors, including their cooperative action in lymphomagenesis. We review our current knowledge about the role of MYC-induced apoptosis in B-cell malignancies, discussing the transcriptional regulation network of MYC and regulatory feedback action of miRs during MYC-driven lymphomagenesis. More importantly, the finding of new modulators of apoptosis now enabling researchers to translate the discoveries that have been made in the laboratory into clinical practice to positively impact human health.

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“…Multifactorial reprogramming to acidification of melanoma tumor microenvironment. The pH and oxygen microenvironment work together with genetic and metabolic pathways to promote melanoma proliferation and metastasis progression [176] . HIF-1α: hypoxia-inducible factor-1 alpha; mTOR: mammalian target of rapamycin Sustained ERK phosphorylation inhibits MITF keeping its levels low leading to proliferation.…”

Section: Microphthalmia-associated Transcription Factormentioning

confidence: 99%

Overview of genetic signaling pathway interactions within cutaneous malignancies

Maner¹,

Dupuis²,

Su³

et al. 2020

JCMT

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Melanoma and non-melanoma cutaneous malignancies are some of the leading causes of cancer-related death in the United States. Though melanoma is more known to have a high mortality rate, the total mortality per year is nearly equal for between melanoma and non-melanoma skin cancer. Moreover, the non-melanoma types of cutaneous malignancies have potential to become locally invasive and even metastasize with very little to no treatment options when advanced. The development of these malignancies involves various genetic pathways through the four hallmarks of cancer development: malignant cell growth, apoptosis evasion, the use of supporting stroma and vascularization, and modulating and promoting an inadequate immune response. The genetic signaling pathways of basal cell carcinoma, squamous cell carcinoma, verrucous carcinoma, basosquamous cell carcinoma, melanoma, and cutaneous T-cell lymphoma interact with each other through genetic predisposition as well as with environmental exposures. Furthermore, solar ultraviolet radiation and chronic inflammatory states are found to initiate the progression of many of these cutaneous malignancies. This paper includes validated models of genetic pathways, emerging pathways, and crosstalk between genetic pathways through the four hallmarks of cancer development. Moreover, unlike most reviews addressing oncogenetics of the well-recognized, as well as newly dynamic, interrelated, interactive, complex, and adaptive flux states.

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Metabolic Plasticity of Melanoma Cells and Their Crosstalk With Tumor Microenvironment

Cited by 77 publications

References 242 publications

Metabolomics of primary cutaneous melanoma and matched adjacent extratumoral microenvironment

Metabolomics of primary cutaneous melanoma and matched adjacent extratumoral microenvironment

Insights about MYC and Apoptosis in B-Lymphomagenesis: An Update from Murine Models

Overview of genetic signaling pathway interactions within cutaneous malignancies

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