Effect of polyphenols on glucose and lactate transport by breast cancer cells

Martel, Fátima; Guedes, Marta; Keating, Elisa

doi:10.1007/s10549-016-3794-z

Cited by 41 publications

(49 citation statements)

References 81 publications

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“…As expected, ER6 cells overexpressed lactate transporter MCT-4, which transports lactic acid to the culture medium. This is similar as reported in other's research that drug resistant cells with higher glycolysis produce more lactic acid and/or overexpressed MCT-4 14 , 27 - 30 . Our data indicated that ER6 cells up-regulated GLUT1 and MCT-4 to increase the uptake of glucose and transportation of lactic acid through the membrane, which was observed as increased glycolysis rate in ER6 cells.…”

Section: Discussionsupporting

confidence: 92%

Combined Inhibitions of Glycolysis and AKT/autophagy Can Overcome Resistance to EGFR-targeted Therapy of Lung Cancer

Ye¹,

Wang²,

Wan³

et al. 2017

J. Cancer

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Efficacy of EGFR-targeted tyrosine kinase inhibitors (TKIs), such as erlotinib, to treat human non-small cell lung cancers (NSCLCs) with activating mutations in EGFR is not persistent due to drug resistance. Reprogramming in energy (especially glucose) metabolism plays an important role in development and progression of acquired resistance in cancer cells. We hypothesize that glucose metabolism in EGFR-TKI sensitive HCC827 cells and erlotinib-resistant sub-line of HCC827 (which we name it as erlotinib-resistant 6, ER6 cells in this study) is different and targeting glucose metabolism might be a treatment strategy for erlotinib-resistant NSCLCs. In this study, we found increased glucose uptakes, significant increase in glycolysis rate and overexpression of glucose transporter 1 in ER6 cells compared to its parental cells HCC827. We also found AKT and autophagy of ER6 cells were more activated than HCC827 cells after glucose starvation. Combining glucose deprivation and AKT or autophagy inhibitor could synergize and overcome the acquired resistance against EGFR-targeted therapy for NSCLCs. Our data suggest that the combinations of inhibitors of AKT or autophagy together with glucose deprivation could be novel treatment strategies for NSCLC with acquired resistance to targeted therapy.

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Section: Discussionsupporting

confidence: 92%

Combined Inhibitions of Glycolysis and AKT/autophagy Can Overcome Resistance to EGFR-targeted Therapy of Lung Cancer

Ye¹,

Wang²,

Wan³

et al. 2017

J. Cancer

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“…Intracellular sodium could alter ΔΨm via sodiumcalcium and sodium-hydrogen exchangers [16,17]. However, low glucose might not regulate ΔΨm; glucose transporter 1 is also expressed in breast cancer cells and is an important energy regulator and therapeutic target [18]. Further experiments may reveal other effects of SGLT2 inhibitors on cancer cells and explore combination treatment with SGLT2 inhibitor, metformin and GLP-1.…”

Section: Discussionmentioning

confidence: 99%

SGLT2 inhibitor ipragliflozin attenuates breast cancer cell proliferation

et al. 2020

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Cancer is currently one of the major causes of death in patients with type 2 diabetes mellitus. We previously reported the beneficial effects of the glucagon-like peptide-1 receptor agonist exendin-4 against prostate and breast cancer. In the present study, we examined the anti-cancer effect of the sodium-glucose cotransporter 2 (SGLT2) inhibitor ipragliflozin using a breast cancer model. In human breast cancer MCF-7 cells, SGLT2 expression was detected using both RT-PCR and immunohistochemistry. Ipragliflozin at 1-50 μM significantly and dose-dependently suppressed the growth of MCF-7 cells. BrdU assay also revealed that ipragliflozin attenuated the proliferation of MCF-7 cells in a dose-dependent manner. Because the effect of ipragliflozin against breast cancer cells was completely canceled by knocking down SGLT2, ipragliflozin could act via inhibiting SGLT2. We next measured membrane potential and whole-cell current using the patch clamp technique. When we treated MCF-7 cells with ipragliflozin or glucose-free medium, membrane hyperpolarization was observed. In addition, glucose-free medium and knockdown of SGLT2 by siRNA suppressed the glucose-induced whole-cell current of MCF-7 cells, suggesting that ipragliflozin inhibits sodium and glucose cotransport through SGLT2. Furthermore, JC-1 green fluorescence was significantly increased by ipragliflozin, suggesting the change of mitochondrial membrane potential. These findings suggest that the SGLT2 inhibitor ipragliflozin attenuates breast cancer cell proliferation via membrane hyperpolarization and mitochondrial membrane instability.

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“…Several distinct mechanisms are involved in their anticarcinogenic effect in breast cancer: interference with redox balance, pro-apoptotic effect, cell cycle arrest, activation of autophagy, inhibition of angiogenesis, anti-inflammatory effect, anti-estrogenic effect, changes in ER expression, aromatase modulation, interference with HER2 signaling, and effect on microbiota [131,132]. Additionally, some polyphenols interfere with glucose cellular uptake by breast cancer cells [133,134], as next described.…”

Section: Polyphenolsmentioning

confidence: 94%

Targeting Glucose Transporters for Breast Cancer Therapy: The Effect of Natural and Synthetic Compounds

Barbosa

Martel

2020

Cancers

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Reprogramming of cellular energy metabolism is widely accepted to be a cancer hallmark. The deviant energetic metabolism of cancer cells-known as the Warburg effect-consists in much higher rates of glucose uptake and glycolytic oxidation coupled with the production of lactic acid, even in the presence of oxygen. Consequently, cancer cells have higher glucose needs and thus display a higher sensitivity to glucose deprivation-induced death than normal cells. So, inhibitors of glucose uptake are potential therapeutic targets in cancer. Breast cancer is the most commonly diagnosed cancer and a leading cause of cancer death in women worldwide. Overexpression of facilitative glucose transporters (GLUT), mainly GLUT1, in breast cancer cells is firmly established, and the consequences of GLUT inhibition and/or knockout are under investigation. Herein we review the compounds, both of natural and synthetic origin, found to interfere with uptake of glucose by breast cancer cells, and the consequences of interference with that mechanism on breast cancer cell biology. We will also present data where the interaction with GLUT is exploited in order to increase the efficiency or selectivity of anticancer agents, in breast cancer cells.

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Effect of polyphenols on glucose and lactate transport by breast cancer cells

Cited by 41 publications

References 81 publications

Combined Inhibitions of Glycolysis and AKT/autophagy Can Overcome Resistance to EGFR-targeted Therapy of Lung Cancer

Combined Inhibitions of Glycolysis and AKT/autophagy Can Overcome Resistance to EGFR-targeted Therapy of Lung Cancer

SGLT2 inhibitor ipragliflozin attenuates breast cancer cell proliferation

Targeting Glucose Transporters for Breast Cancer Therapy: The Effect of Natural and Synthetic Compounds

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