Role of MicroRNAs in the Warburg Effect and Mitochondrial Metabolism in Cancer

Jin, L; Chen, Wei

doi:10.7314/apjcp.2014.15.17.7015

Cited by 22 publications

(5 citation statements)

References 61 publications

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“…Recently, it has been noted that metastatic cells have an increased dependency on glycolytic pathways while down-regulating pathways involved in oxidative phosphorylation (Sottnik et al, 2011;Jin and Wei, 2014). This is a further enhancement of the Warburg effect which states that tumor cells become dependent on glycolysis and decrease their oxygen utilization as they become more aggressive (Zhao et al, 2013;Jin and Wei, 2014). These metabolic differences arise as a result of a fundamental defect in the tumor mitochondrial electron transport chain which leads to increased steady state levels of pro-oxidants (Nakashima et al, 1984).…”

Section: Discussionmentioning

confidence: 99%

2-deoxy-D-Glucose Synergizes with Doxorubicin or L-Buthionine Sulfoximine to Reduce Adhesion and Migration of Breast Cancer Cells

Mustafa¹,

Mahmoud²,

Alhudhud³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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Background: Cancer metastasis depends on cell motility which is driven by cycles of actin polymerization and depolymerization. Reactive oxygen species (ROS) and metabolic oxidative stress have long been associated with cancer. ROS play a vital role in regulating actin dynamics that are sensitive to oxidative modification. The current work aimed at studying the effects of sub-lethal metabolic oxidative stress on actin cytoskeleton, focal adhesion and cell migration. Materials and Methods: T47D human breast cancer cells were treated with 2-deoxy-D-glucose (2DG), L-buthionine sulfoximine (BSO), or doxorubicin (DOX), individually or in combination, and changes in intracellular total glutathione and malondialdehyde (MDA) levels were measured. The expression of three major antioxidant enzymes was studied by immunoblotting, and cells were stained with fluorescentphalloidin to evaluate changes in F-actin organization. In addition, cell adhesion and degradation ability were measured. Cell migration was studied using wound healing and transwell migration assays. Results: Our results show that treating T47D human breast cancer cells with drug combinations (2DG/BSO, 2DG/DOX, or BSO/DOX) decreased intracellular total glutathione and increased oxidized glutathione, lipid peroxidation, and cytotoxicity. In addition, the drug combinations caused a reduction in cell area and mitotic index, prophase arrest and a decreased ability to form invadopodia. The formation of F-actin aggregates was increased in treated T47D cells. Moreover, combination therapy reduced cell adhesion and the rate of cell migration. Conclusions: Our results suggest that exposure of T47D breast cancer cells to combination therapy reduces cell migration via effects on metabolic oxidative stress.

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Section: Discussionmentioning

confidence: 99%

2-deoxy-D-Glucose Synergizes with Doxorubicin or L-Buthionine Sulfoximine to Reduce Adhesion and Migration of Breast Cancer Cells

Mustafa¹,

Mahmoud²,

Alhudhud³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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“…Deregulations of microRNA expression have been associated with tumor development, progression, metastasis, and therapeutic responses [81]. Notably, miRNAs are shown to mediate metabolic phenotypes through the regulation of glycolytic enzymes and mitochondria metabolism [82]. Growing evidence suggests a reciprocal connection between ROS signaling and the microRNA pathway, resulting in diverse biological effects in cancer cells [83].…”

Section: Ros-responsive Mirnasmentioning

confidence: 99%

Reactive Oxygen Species, Metabolic Plasticity, and Drug Resistance in Cancer

Bhardwaj

2020

IJMS

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The metabolic abnormality observed in tumors is characterized by the dependence of cancer cells on glycolysis for their energy requirements. Cancer cells also exhibit a high level of reactive oxygen species (ROS), largely due to the alteration of cellular bioenergetics. A highly coordinated interplay between tumor energetics and ROS generates a powerful phenotype that provides the tumor cells with proliferative, antiapoptotic, and overall aggressive characteristics. In this review article, we summarize the literature on how ROS impacts energy metabolism by regulating key metabolic enzymes and how metabolic pathways e.g., glycolysis, PPP, and the TCA cycle reciprocally affect the generation and maintenance of ROS homeostasis. Lastly, we discuss how metabolic adaptation in cancer influences the tumor’s response to chemotherapeutic drugs. Though attempts of targeting tumor energetics have shown promising preclinical outcomes, the clinical benefits are yet to be fully achieved. A better understanding of the interaction between metabolic abnormalities and involvement of ROS under the chemo-induced stress will help develop new strategies and personalized approaches to improve the therapeutic efficiency in cancer patients.

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“…Based on the size of the transcripts, ncRNAs are classified into small ncRNAs (shorter than 200 nucleotides) and long ncRNAs (lncRNAs; longer than 200 nucleotides). Small ncRNAs include microRNAs (miRNAs), piwi‐interacting RNAs (piRNAs), and small nucleolar RNAs (snoRNAs) , and it is widely appreciated that small ncRNAs, particularly miRNAs, regulate a broad spectrum of biological processes, including cancer metabolism . The functions of lncRNAs in an array of biological processes have been established ; however, their roles in the regulation of metabolism and energy homeostasis remain largely elusive.…”

Section: Introductionmentioning

confidence: 99%

Long non‐coding RNAs in cancer metabolism

Xiao

Gan

2016

BioEssays

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Altered cellular metabolism is an emerging hallmark of cancer. Accumulating recent evidence links long non-coding RNAs (lncRNAs), a still poorly understood class of non-coding RNAs, to cancer metabolism. Here we review the emerging findings on the functions of lncRNAs in cancer metabolism, with particular emphasis on how lncRNAs regulate glucose and glutamine metabolism in cancer cells, discuss how lncRNAs regulate various aspects of cancer metabolism through their cross-talk with other macromolecules, explore the mechanistic conceptual framework of lncRNAs in reprogramming metabolism in cancers, and highlight the challenges in this field. A more in-depth understanding of lncRNAs in cancer metabolism may enable the development of novel and effective therapeutic strategies targeting cancer metabolism.

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Role of MicroRNAs in the Warburg Effect and Mitochondrial Metabolism in Cancer

Cited by 22 publications

References 61 publications

2-deoxy-D-Glucose Synergizes with Doxorubicin or L-Buthionine Sulfoximine to Reduce Adhesion and Migration of Breast Cancer Cells

2-deoxy-D-Glucose Synergizes with Doxorubicin or L-Buthionine Sulfoximine to Reduce Adhesion and Migration of Breast Cancer Cells

Reactive Oxygen Species, Metabolic Plasticity, and Drug Resistance in Cancer

Long non‐coding RNAs in cancer metabolism

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