Quercetin and epigallocatechin gallate inhibit glucose uptake and metabolism by breast cancer cells by an estrogen receptor-independent mechanism

Moreira, Liliana; Araújo, Isabel M.; Costa, Tito Vanelli; Correia-Branco, Ana; Faria, Ana; Martel, Fátima; Keating, Elisa

doi:10.1016/j.yexcr.2013.05.001

Cited by 83 publications

(70 citation statements)

References 39 publications

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“…Its activation is dependent on insulin secretion and takes place mainly through the activation of the PI3K/AKT pathway (Charron et al, ; Grillo et al, ). Recently, it has been demonstrated that GLUT4 is expressed in breast cancer cells (Medina et al, ; Garrido et al, ; Moreira et al, ), and despite little is still known about the involvement of this transporter in cancer biology and metabolism (Knobbe et al, ; Bachman et al, ; Pedrero et al, ; Caro‐Maldonado and Munoz‐Pinedo, ), it has been demonstrated the expression of this glucose transporter in, both triple negative and non‐triple negative, breast cancer samples (Yang et al, ).…”

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confidence: 99%

Loss of GLUT4 Induces Metabolic Reprogramming and Impairs Viability of Breast Cancer Cells

Garrido

Osorio

Morán

et al. 2014

Journal Cellular Physiology

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Metabolic reprogramming strategies focus on the normalization of metabolism of cancer cells and constitute promising targets for cancer treatment. Here, we demonstrate that the glucose transporter 4 (GLUT4) has a prominent role in basal glucose uptake in MCF7 and MDA-MB-231 breast cancer cells. We show that shRNA-mediated down-regulation of GLUT4 diminishes glucose uptake and induces metabolic reprogramming by reallocating metabolic flux to oxidative phosphorylation. This reallocation is reflected on an increased activity of the mitochondrial oxidation of pyruvate and lower lactate release. Altogether, GLUT4 inhibition compromises cell proliferation and critically affects cell viability under hypoxic conditions, providing proof-of-principle for the feasibility of using pharmacological approaches to inhibit GLUT4 in order to induce metabolic reprogramming in vivo in breast cancer models.

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confidence: 99%

Loss of GLUT4 Induces Metabolic Reprogramming and Impairs Viability of Breast Cancer Cells

Garrido

Osorio

Morán

et al. 2014

Journal Cellular Physiology

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“…Glucose uptake. In previous experiments, uptake of [ 3 H]-DG in MCF-7 cells was linear with time for up to 6 min of incubation [Moreira et al, 2013]. Thus, in the present study, cells were incubated with [ 3 H]-DG for 6 min, in order to determine initial rates of uptake.…”

Section: Short-term Exposurementioning

confidence: 83%

Effects of Environmental Pollutants on MCF-7 Cells: A Metabolic Approach

et al. 2016

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Several environmental pollutants (EPs) have been associated with biological and molecular processes leading to adverse human health effects, including different types of cancer. Nevertheless, the effects exerted on tumor glucose metabolism are unclear. To evaluate the effects on cellular and molecular mechanisms, namely glucose metabolism, MCF-7 cells were exposed to EPs during short- and long-term exposures. The effect of both, organochlorine pesticides and plasticizing agents, on glucose uptake by MCF-7 cells was not dose-dependent and was affected by time of exposure. The ΣHCH and BPA increased glucose uptake after 20 min. Long-term exposure to 250 nM of organochlorine pesticides (p,p'-DDE and ΣHCH) and BPA increased cell proliferation. However, only the organochlorine pesticides were able to increase lactate production, without a concomitant higher glucose uptake or glycolytic enzymes transcription. Given their distinct persistent profiles, the biological significance of their exposure should be considered accordingly. J. Cell. Biochem. 118: 366-375, 2017. © 2016 Wiley Periodicals, Inc.

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“…Both compounds at a concentration of 100 µM were able to reduce lactate production in MCF7 cells and decreased MCF7 cell viability and proliferation. 25 …”

Section: Natural Glut Inhibitorsmentioning

confidence: 99%

Anticancer agents interacting with membrane glucose transporters

2016

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The altered metabolism observed in cancer cells generally consists in increased glucose uptake and glycolytic activity. This is associated with an overexpression of glucose transporter proteins (GLUTs), which facilitate glucose uptake across the plasma membrane and play a crucial role in the survival of cancer cells. Therefore GLUTs are considered as suitable targets for the treatment of cancer. Herein we review some of the most relevant GLUT inhibitors that have been recently developed as prospective anticancer agents.

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Quercetin and epigallocatechin gallate inhibit glucose uptake and metabolism by breast cancer cells by an estrogen receptor-independent mechanism

Cited by 83 publications

References 39 publications

Loss of GLUT4 Induces Metabolic Reprogramming and Impairs Viability of Breast Cancer Cells

Loss of GLUT4 Induces Metabolic Reprogramming and Impairs Viability of Breast Cancer Cells

Effects of Environmental Pollutants on MCF-7 Cells: A Metabolic Approach

Anticancer agents interacting with membrane glucose transporters

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