Glucose Metabolism in Cancer

Bose, Sminu; Le, Anne

doi:10.1007/978-3-319-77736-8_1

Cited by 169 publications

(126 citation statements)

References 36 publications

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“…The aberrant glucose metabolism in cancer cells associates with cell proliferation and resistance to radiation and chemotherapy. Tumor cells require higher rates of glucose uptake, and have higher catabolite uptake and use [65,66]. In breast cancer, CCR5 engagement induces Akt phosphorylation, stimulating glucose uptake, glycolysis, the pentose phosphate pathway, fatty acid synthesis, and glutamine metabolism [55].…”

Section: Deregulated Cellular Energetics (Metabolic Reprogramming)mentioning

confidence: 99%

The CCL5/CCR5 Axis in Cancer Progression

Aldinucci

Borghese

Casagrande

2020

Cancers

285

191

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Tumor cells can “hijack” chemokine networks to support tumor progression. In this context, the C-C chemokine ligand 5/C-C chemokine receptor type 5 (CCL5/CCR5) axis is gaining increasing attention, since abnormal expression and activity of CCL5 and its receptor CCR5 have been found in hematological malignancies and solid tumors. Numerous preclinical in vitro and in vivo studies have shown a key role of the CCL5/CCR5 axis in cancer, and thus provided the rationale for clinical trials using the repurposed drug maraviroc, a CCR5 antagonist used to treat HIV/AIDS. This review summarizes current knowledge on the role of the CCL5/CCR5 axis in cancer. First, it describes the involvement of the CCL5/CCR5 axis in cancer progression, including autocrine and paracrine tumor growth, ECM (extracellular matrix) remodeling and migration, cancer stem cell expansion, DNA damage repair, metabolic reprogramming, and angiogenesis. Then, it focuses on individual hematological and solid tumors in which CCL5 and CCR5 have been studied preclinically. Finally, it discusses clinical trials of strategies to counteract the CCL5/CCR5 axis in different cancers using maraviroc or therapeutic monoclonal antibodies.

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Section: Deregulated Cellular Energetics (Metabolic Reprogramming)mentioning

confidence: 99%

The CCL5/CCR5 Axis in Cancer Progression

Aldinucci

Borghese

Casagrande

2020

Cancers

285

191

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“…Recent studies revealed that KD can also be applied to the treatment of some metabolic or endocrine diseases such as obesity, diabetes and hypertension [11,12]. As we know, malignant tumors were also regarded as a metabolic disease due to their altered glucose metabolism, which was tumor cells preferentially utilize glycolysis instead of oxidative phosphorylation to generate energy and other metabolites [13]. Therefore, KD is becoming a promising adjuvant support therapy for cancer treatment in recent years [14].…”

Section: Introductionmentioning

confidence: 99%

Ketogenic diet promotes apoptosis of tumor cells and inhibits tumor growth through inhibiting Wnt1/β-catenin signaling pathway in mouse xenograft models of human colon cancer

Wang¹,

Qiu²,

Wu³

et al. 2020

Preprint

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Background: High-fat, low-carbohydrate and adequate-protein ketogenic diets (KD) are expected to become an effective adjunct therapy for cancer patients. However, the direct effects of KD on tumor cells and the underlying mechanisms are elusive. In this study, the nude mouse models of subcutaneous transplanted human colon cancer cells were established and applied to study the effects and mechanisms of KD on the growth of subcutaneous tumors in nude mice.Methods: Male nude mice were injected subcutaneously with human colon cancer HCT-116 cell line to construct a subcutaneous tumor model of human colon cancer. The successfully constructed subcutaneous tumor mice were divided into normal diet group and KD group. The mice were anesthetized and euthanized after 30 days of feeding, the subcutaneous tumor tissues were collected, and the size of tumors was measured and weighed. HE staining was used to observe the pathological changes of subcutaneous tumor tissues in normal feeding group and KD group. TUNEL staining was used to detect the level of apoptosis in tumor tissue. Immunohistochemistry of subcutaneous tumor tissues was used to detect the expression levels of Wnt-1 and β-catenin. In addition, RT-qPCR and western blotting were applied to detect the expression levels of Wnt1/β-catenin signaling pathway-related proteins.Results: After 30 days of normal diet and KD feeding, the subcutaneous tumor tissues of human colon cancer mice were taken out for various assays. The results of tumor size measurement showed that the tumor size and weight of KD group were significantly smaller than that of the normal diet group. HE staining showed that the pathological characteristics of colon tumor tissue in the KD group were significantly improved, and the infiltration of inflammatory cells was reduced. TUNEL staining showed that the apoptosis level of tumor cells in the KD group was significantly increased compared to the normal diet group. RT-qPCR and western blotting revealed that the expression of pro-apoptotic proteins such as caspase 3，caspase 9 and Bax were increased（P < 0.01）, while the expression of anti-apoptotic protein such as Bcl-2 or survivin was decreased （P < 0.01）. Furthermore, the expression of Wnt1/β-catenin signaling pathway-related proteins including Wnt1 and β-catenin were largely reduced after 30 days of KD feeding compared to normal feeding group （P < 0.01）.Conclusions: Ketogenic diets (KD) promotes apoptosis of human colon cancer subcutaneous tumor cells and inhibits the growth of tumor by inhibiting Wnt1/β-catenin signaling pathway in mouse subcutaneous tumor models of human colon cancer.

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“…Most normal tissues get energy through aerobic oxidation of sugar, and glycolysis occurs only in the absence of oxygen (28). The main approach for tumor cells to get energy is glycolysis, and the product of glycolysis is lactic acid (29).…”

Section: Introductionmentioning

confidence: 99%

LncRNA-BLACAT1 Facilitates Proliferation, Migration and Aerobic Glycolysis of Pancreatic Cancer Cells by Repressing CDKN1C via EZH2-Induced H3K27me3

et al. 2020

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Objective: To investigate the role of lncRNA-BLACAT1 in promoting H3K27 trimethylation of CDKN1C gene by recruiting EZH2 to regulate CCNE on glycolysis and mitochondrial oxidative phosphorylation of pancreatic cancer (PC) cells. Methods: Following bioinformatic prediction, EZH2 and BLACAT1 in PC cells were interfered, and cells proliferation, migration and invasion in each group were detected. Western blotting detected the expression of key proteins of mitochondrial complex. The sub-cellular localization of BLACAT1 was tested, followed by testing the binding of CDKN1C and BLACAT1 with EZH2, followed by in vivo verification. Results: Based on bioinformatic prediction, EZH2 and BLACAT1 were highly expressed in PC, while CDKN1C was lowly expressed (all P < 0.05). Interference with EZH2 and BLACAT1 inhibited cell proliferation, migration and aerobic glycolysis, and promoted mitochondrial oxidative phosphorylation (all P < 0.05). BLACAT1 promoted H3K27 trimethylation of CDKN1C through recruiting EZH2 (all P < 0.05). In vivo results showed that BLACAT1 interference inhibited tumor formation (all P < 0.05). Conclusion: Interference with BLACAT1 inhibits H3K27 trimethylation of CDKN1C gene by blocking EZH2 recruitment to promote CDKN1C expression and inhibit CCNE expression, thus suppressing PC cell proliferation, migration and aerobic glycolysis, and promoting mitochondrial oxidative phosphorylation.

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Glucose Metabolism in Cancer

Cited by 169 publications

References 36 publications

The CCL5/CCR5 Axis in Cancer Progression

The CCL5/CCR5 Axis in Cancer Progression

Ketogenic diet promotes apoptosis of tumor cells and inhibits tumor growth through inhibiting Wnt1/β-catenin signaling pathway in mouse xenograft models of human colon cancer

LncRNA-BLACAT1 Facilitates Proliferation, Migration and Aerobic Glycolysis of Pancreatic Cancer Cells by Repressing CDKN1C via EZH2-Induced H3K27me3

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