miRNAs link metabolic reprogramming to oncogenesis

Hatziapostolou, Maria; Polytarchou, Christos; Iliopoulos, Dimitrios

doi:10.1016/j.tem.2013.03.002

Cited by 70 publications

(62 citation statements)

References 256 publications

(161 reference statements)

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“…The metabolic reprogramming of cancer cells is achieved through a complex interplay of regulatory networks involving phosphatidylinositide 3-kinase (PI3K), mTOR, protein kinase B (Akt), PTEN and 5' AMP-activated protein kinase (AMPK). While many miRNAs regulate glucose, lipid and the metabolism of amino acids by modulating gene transcription, the lack of information on major metabolic processes in the mammary glands has meant that metabolic reprograming by miRNAs in breast cancer has not been studied in detail [8]. It is well known that cancer cells use mechanisms of aerobic energy production rather than oxidative phosphorylation [7,15]; most fundamental metabolic processes such as increased rates of glucose uptake and glycolysis, suppressed gluconeogenesis, and lactic acid fermentation are altered.…”

Section: Mirnas Mediate Metabolic Reprogramming In Breast Cancermentioning

confidence: 99%

“…The dysregulation of miRNAs affects the rate of glycolysis [6], and miRNAs such as miR-129, which enhances GLUT-1 expression, therefore contributing to the Warburg effect [7]. Malignant transformation is also associated with excessive glucose uptake, de novo fatty acid synthesis, glutaminolysis, altered lipid metabolism, aerobic glycolysis, and an increase of reactive oxygen species (ROS) [8].…”

Section: Mirnas Mediate Metabolic Reprogramming In Breast Cancermentioning

confidence: 99%

“…The mechanism(s) remains to be established by which enhanced glycolytic activity and increased ROS are activated; the latter directly suppresses aerobic glycolysis by inhibiting pyruvate kinase (PKM2) and inducing NADPH production. This facilitates antioxidant synthesis and thus permits the accumulation of glycolytic intermediates [8]. How signaling pathways control energy metabolism is an important question, since studying metabolic pathways may yield new targets in treating drug-resistant and metastatic breast cancers [11,12].…”

Section: Mirnas Mediate Metabolic Reprogramming In Breast Cancermentioning

confidence: 99%

“…The first miRNA found to be associated with lipid metabolism was miR-122 [34], which has been implicated in the increased synthesis of lipids and cholesterol-rich membranes in cancer cells [35]. The inhibition of miR-122 (a tumor suppressor) disrupts lipid storage and lipid metabolism in breast cancer cells [8,32,41]. In addition, glutathione S-transferase Pi 1…”

Section: Role Of Mirnas In Homeostasis and Metabolism Of Lipidsmentioning

confidence: 99%

“…PGI, a cytosolic enzyme that catalyzes the interconversion of glucose-6-phosphate and fructose-6-phosphate, plays a fundamental role in gluconeogenesis and glycolysis. PGI regulates miR-200 family expression, which directly affects the EMT in breast cancer [8,27]. In contrast to the intracellular level of miR-122, which does not significantly differ whether metastatic or nonmetastatic, the level of exosomal (circulating) miR-122 is correlated with the metastatic capacity of breast cancer [28,29].…”

Section: Role Of Mirnas In Glycolysismentioning

confidence: 99%

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Metabolic Reprogramming of Triple-Negative Breast Cancer: The Role of miRNAs

Qattan¹

2017

microRNA Diagnostics and Therapeutics

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Section: Mirnas Mediate Metabolic Reprogramming In Breast Cancermentioning

confidence: 99%

Section: Mirnas Mediate Metabolic Reprogramming In Breast Cancermentioning

confidence: 99%

Section: Mirnas Mediate Metabolic Reprogramming In Breast Cancermentioning

confidence: 99%

Section: Role Of Mirnas In Homeostasis and Metabolism Of Lipidsmentioning

confidence: 99%

Section: Role Of Mirnas In Glycolysismentioning

confidence: 99%

See 3 more Smart Citations

Metabolic Reprogramming of Triple-Negative Breast Cancer: The Role of miRNAs

Qattan¹

2017

microRNA Diagnostics and Therapeutics

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EMT‐ and MET‐related processes in nonepithelial tumors: importance for disease progression, prognosis, and therapeutic opportunities

2017

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The epithelial‐to mesenchymal (EMT) process is increasingly recognized for playing a key role in the progression, dissemination, and therapy resistance of epithelial tumors. Accumulating evidence suggests that EMT inducers also lead to a gain in mesenchymal properties and promote malignancy of nonepithelial tumors. In this review, we present and discuss current findings, illustrating the importance of EMT inducers in tumors originating from nonepithelial/mesenchymal tissues, including brain tumors, hematopoietic malignancies, and sarcomas. Among these tumors, the involvement of mesenchymal transition has been most extensively investigated in glioblastoma, providing proof for cell autonomous and microenvironment‐derived stimuli that provoke EMT‐like processes that regulate stem cell, invasive, and immunogenic properties as well as therapy resistance. The involvement of prominent EMT transcription factor families, such as TWIST, SNAI, and ZEB, in promoting therapy resistance and tumor aggressiveness has also been reported in lymphomas, leukemias, and sarcomas. A reverse process, resembling mesenchymal‐to‐epithelial transition (MET), seems particularly relevant for sarcomas, where (partial) epithelial differentiation is linked to less aggressive tumors and a better patient prognosis. Overall, a hybrid model in which more stable epithelial and mesenchymal intermediates exist likely extends to the biology of tumors originating from sources other than the epithelium. Deeper investigation and understanding of the EMT/MET machinery in nonepithelial tumors will shed light on the pathogenesis of these tumors, potentially paving the way toward the identification of clinically relevant biomarkers for prognosis and future therapeutic targets.

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Crosstalk between metabolic reprogramming and epigenetics in cancer: updates on mechanisms and therapeutic opportunities

Jia

et al. 2022

Cancer Communications

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Reversible, spatial, and temporal regulation of metabolic reprogramming and epigenetic homeostasis are prominent hallmarks of carcinogenesis. Cancer cells reprogram their metabolism to meet the high bioenergetic and biosynthetic demands for vigorous proliferation. Epigenetic dysregulation is a common feature of human cancers, which contributes to tumorigenesis and maintenance of the malignant phenotypes by regulating gene expression. The epigenome is sensitive to metabolic changes. Metabolism produces various metabolites that are substrates, cofactors, or inhibitors of epigenetic enzymes. Alterations in metabolic pathways and fluctuations in intermediate metabolites convey information regarding the intracellular metabolic status into the nucleus by modulating the activity of epigenetic enzymes and thus remodeling the epigenetic landscape, inducing transcriptional responses to heterogeneous metabolic requirements. Cancer metabolism is regulated by epigenetic machinery at both transcriptional and post‐transcriptional levels. Epigenetic modifiers, chromatin remodelers and non‐coding RNAs are integral contributors to the regulatory networks involved in cancer metabolism, facilitating malignant transformation. However, the significance of the close connection between metabolism and epigenetics in the context of cancer has not been fully deciphered. Thus, it will be constructive to summarize and update the emerging new evidence supporting this bidirectional crosstalk and deeply assess how the crosstalk between metabolic reprogramming and epigenetic abnormalities could be exploited to optimize treatment paradigms and establish new therapeutic options. In this review, we summarize the central mechanisms by which epigenetics and metabolism reciprocally modulate each other in cancer and elaborate upon and update the major contributions of the interplays between epigenetic aberrations and metabolic rewiring to cancer initiation and development. Finally, we highlight the potential therapeutic opportunities for hematological malignancies and solid tumors by targeting this epigenetic‐metabolic circuit. In summary, we endeavored to depict the current understanding of the coordination between these fundamental abnormalities more comprehensively and provide new perspectives for utilizing metabolic and epigenetic targets for cancer treatment.

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miRNAs link metabolic reprogramming to oncogenesis

Cited by 70 publications

References 256 publications

Metabolic Reprogramming of Triple-Negative Breast Cancer: The Role of miRNAs

Metabolic Reprogramming of Triple-Negative Breast Cancer: The Role of miRNAs

EMT‐ and MET‐related processes in nonepithelial tumors: importance for disease progression, prognosis, and therapeutic opportunities

Crosstalk between metabolic reprogramming and epigenetics in cancer: updates on mechanisms and therapeutic opportunities

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