Hypoxic glucose metabolism in glioblastoma as a potential prognostic factor

Toyonaga, Takuya; Yamaguchi, Shigeru; Hirata, Kenji; Kobayashi, Kentaro; Manabe, Osamu; Watanabe, Shirô; Terasaka, Shunsuke; Kobayashi, Hiroyuki; Hattori, Naoya; Shiga, Tohru; Kuge, Yuji; Tanaka, Shinya; Ito, Yoichi M.; Tamaki, Nagara

doi:10.1007/s00259-016-3541-z

Cited by 46 publications

(42 citation statements)

References 40 publications

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“…HIF1α stimulates aerobic glycolysis by inducing the expression of glucose transporters (such as glucose transporter 1, GLUT1) and directly targeting enzymes that regulate glycolysis, such as hexokinase 2 (HK2), phosphoglycerate kinase 1 (PGK1), lactate dehydrogenase A (LDHA), monocarboxylate transporter 4, and pyruvate dehydrogenase lipoamide kinase isozyme 1 (PDK1) [12]. A number of studies have revealed the importance of this metabolic reprogramming in cancer cells [13-17]. …”

Section: Introductionmentioning

confidence: 99%

Propofol Disrupts Aerobic Glycolysis in Colorectal Cancer Cells via Inactivation of the NMDAR-CAMKII-ERK Pathway

Chen

Sun

et al. 2018

Cell Physiol Biochem

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Background/Aims: To investigate the effect of propofol on glucose metabolism in colorectal cancer cells and in an in vivo xenograft model. Methods: Glucose metabolism was assessed by measuring the extracellular acidification rate in HT29 and SW480 colorectal cancer cells. Quantitative real-time PCR and western blot analyses were used to detect mRNA and protein levels, respectively. Intracellular calcium was assessed by using a Fluo-3 AM fluorescence kit. Micro-positron emission tomography/computed tomography (microPET/CT) imaging was used to analyze glucose metabolism in the tumors of the xenograft model. Results: Propofol exposure induced a dose-dependent decrease of aerobic glycolysis in HT29 and SW480 colorectal cancer cells. MicroPET/CT indicated that propofol also inhibited ¹⁸F-FDG uptake in the xenograft model. In addition, hypoxia-inducible factor 1α (HIF1α) was also reduced by propofol dose-dependently. Propofol repressed the NMDAR-CAMKII-ERK pathway to inactivate HIF1α and therefore reduced glycolysis. Conclusion: Propofol inhibited aerobic glycolysis in colorectal cancer cells through the inactivation of the NMDAR-CAMKII-ERK pathway, which may facilitate a better understanding of the use of propofol in the clinical setting.

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Section: Introductionmentioning

confidence: 99%

Propofol Disrupts Aerobic Glycolysis in Colorectal Cancer Cells via Inactivation of the NMDAR-CAMKII-ERK Pathway

Chen

Sun

et al. 2018

Cell Physiol Biochem

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“…More recently, a combination of two radiotracers was used to define a metabolic tumor volume in hypoxia, with the latter expressed as the volume of 18 F-FDG / 18 F-fluoromisonidazole ( 18 F-FMISO) double-positive, and 18 F-FMISO used as a radiotracer of hypoxia. This metabolic tumor volume in hypoxia was a significant predictor of progression-free survival and overall survival in glioblastoma patients (105).…”

Section: Prognosticationmentioning

confidence: 99%

“…In addition to this technical multimodality and the concomitant efforts of using various radiopharmaceuticals to characterize multiple biological targets (61,105), currently used multiparametric imaging also integrates the development and applications of innovative methods of image processing and analysis (120). While common metrics such as standard uptake value (SUV) or BTV or TBR only partially describes the properties of pathological lesions, novel parameters such as shape and uptake heterogeneity may provide additional information on the biological profile associated with tumor aggressiveness or degree of response to specific treatment and, consequently, with prognosis (121).…”

Section: Future Perspectives: Novel Radiotracers and Multimodalitymentioning

confidence: 99%

PET Imaging in Glioblastoma: Use in Clinical Practice

Verger¹,

Langen²

2017

Glioblastoma

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Positron emission tomography (PET) is a nuclear medicine imaging method with increasing relevance for the diagnosis, prognostication, and monitoring of glioblastomas. PET provides additional insight beyond magnetic resonance imaging (MRI) into the biology of gliomas, which can be used for noninvasive grading, differential diagnosis, delineation of tumor extent, planning of surgery, and radiotherapy and post-treatment monitoring. In clinical practice, two classes of radiotracers have been used predominantly for imaging purposes, namely glucose metabolism tracers and amino acid transport tracers. Both classes of tracers can provide information on grading and prognosis of gliomas, but amino acid tracers, which exhibit lower uptake in normal brain tissue, are better suited for delineation of tumor extent, treatment planning, or follow-up than 18 F-2-fluoro-2-deoxy-D-glucose ( 18 F-FDG). Owing to the progress in PET imaging using radiolabeled amino acids in recent years, the Response Assessment in Neuro-Oncology (RANO) working group, an international effort to develop new standardized response criteria for clinical trials in brain tumors, has recently recommended amino acid PET as an additional tool in the diagnostic assessment of brain tumors. PET Imaging in Glioblastomas 156These developments as well as multimodality imaging should improve the diagnostic assessment of these tumors.

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“…c‐Myc directly induces the transcription of genes encoding glycolytic enzymes, including HK‐II, LDHA, PGK1 and GLUTs . Numerous studies have demonstrated the importance of this metabolic reprogramming in cancer cells . Moreover, it was reported that c‐Myc can be regulated by CaMK II to facilitate cancer cell proliferation …”

Section: Introductionmentioning

confidence: 99%

Ketamine inhibits aerobic glycolysis in colorectal cancer cells by blocking the NMDA receptor‐CaMK II‐c‐Myc pathway

Duan

Qing

2020

Clin Exp Pharma Physio

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Aerobic glycolysis plays a crucial role in cancer progression. Ketamine is often used for cancer pain relief in clinical settings. Moreover, ketamine inhibits proliferation and induces apoptosis in many cancer cell types. However, the anti‐tumour mechanism of ketamine is still poorly understood. In the present study, we survey whether and how ketamine inhibits aerobic glycolysis in colon cancer cells. Glycolysis of colon cancer cells was determined by detecting the extracellular acidification rate in HT29 and SW480 cells. Quantitative real‐time PCR was employed to determine mRNA expression. Calcium levels were detected with a Fluo‐3 AM fluorescence kit. Micro‐positron emission tomography/computed tomography (microPET/CT) imaging was employed to assess glycolysis in the tumours of the xenograft model. Ketamine treatment inhibited colon cancer cell viability and migration in HT29 and SW480 cells. Moreover, ketamine decreased aerobic glycolysis and decreased the expression of glycolysis‐related proteins in HT29 and SW480 cells. MicroPET/CT demonstrated that ketamine decreased 18F‐FDG uptake in the xenograft model. In addition, ketamine inhibited c‐Myc expression and CaMK II phosphorylation and decreased calcium levels. Further, dizocilpine (an NMDAR inhibitor), and KN93 (a CaMK II inhibitor), decreased CaMK II phosphorylation, c‐Myc expression, and cancer cell glycolysis; these results were similar to those with ketamine treatment. Furthermore, the anti‐tumour effect of ketamine was counteracted by rapastinel (an NMDAR activator). Ketamine inhibited aerobic glycolysis in colon cancer cells probably by blocking the NMDA receptor‐CaMK II‐c‐Myc pathway, thus attenuating colon cancer cell viability and migration.

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Hypoxic glucose metabolism in glioblastoma as a potential prognostic factor

Cited by 46 publications

References 40 publications

Propofol Disrupts Aerobic Glycolysis in Colorectal Cancer Cells via Inactivation of the NMDAR-CAMKII-ERK Pathway

Propofol Disrupts Aerobic Glycolysis in Colorectal Cancer Cells via Inactivation of the NMDAR-CAMKII-ERK Pathway

PET Imaging in Glioblastoma: Use in Clinical Practice

Ketamine inhibits aerobic glycolysis in colorectal cancer cells by blocking the NMDA receptor‐CaMK II‐c‐Myc pathway

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