Correlation of Glut-1 glucose transporter expression with [18F]FDG uptake in non-small cell lung cancer

Higashi, Kõtarõ; Ueda, Yoshimichi; Sakurai, Aya; MingWang, Xiao; Xu, Linfeng; Murakami, Manabu; Seki, Hidetoshi; Oguchi, Manabu; Taki, Suzuka; Nambu, Yoshihiro; Tonami, Hisao; Katsuda, Shogo; Yamamoto, Ikuo

doi:10.1007/s002590000367

Cited by 179 publications

(133 citation statements)

References 14 publications

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“…carcinomas (Higashi et al, 2002), 57 cervical carcinomas (Yen et al, 2004), and 17 ovarian carcinomas (Kurokawa et al, 2004), while a non-significant association was found in two studies of pancreatic carcinoma (Higashi et al, 1998(Higashi et al, , 2000. Other studies have found no association between glucose uptake and GLUT1 expression (Brown et al, 1999).…”

Section: Glut Expression In Tumorsmentioning

confidence: 87%

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Molecular and cellular regulation of glucose transporter (GLUT) proteins in cancer

Macheda

Rogers

Best

2004

Journal Cellular Physiology

1,035

893

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Malignant cells are known to have accelerated metabolism, high glucose requirements, and increased glucose uptake. Transport of glucose across the plasma membrane of mammalian cells is the first rate-limiting step for glucose metabolism and is mediated by facilitative glucose transporter (GLUT) proteins. Increased glucose transport in malignant cells has been associated with increased and deregulated expression of glucose transporter proteins, with overexpression of GLUT1 and/or GLUT3 a characteristic feature. Oncogenic transformation of cultured mammalian cells causes a rapid increase of glucose transport and GLUT1 expression via interaction with GLUT1 promoter enhancer elements. In human studies, high levels of GLUT1 expression in tumors have been associated with poor survival. Studies indicate that glucose transport in breast cancer is not fully explained by GLUT1 or GLUT3 expression, suggesting involvement of another glucose transporter. Recently, a novel glucose transporter protein, GLUT12, has been found in breast and prostate cancers. In human breast and prostate tumors and cultured cells, GLUT12 is located intracellularly and at the cell surface. Trafficking of GLUT12 to the plasma membrane could therefore contribute to glucose uptake. Several factors have been implicated in the regulation of glucose transporter expression in breast cancer. Hypoxia can increase GLUT1 levels and glucose uptake. Estradiol and epidermal growth factor, both of which can play a role in breast cancer cell growth, increase glucose consumption. Estradiol and epidermal growth factor also increase GLUT12 protein levels in cultured breast cancer cells. Targeting GLUT12 could provide novel methods for detection and treatment of breast and prostate cancer.

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Section: Glut Expression In Tumorsmentioning

confidence: 87%

“…A more recent study has confirmed this finding (Ravazoula et al, 2003). In lung and ovarian carcinoma, increased GLUT1 expression has also been associated with a lower degree of tumor differentiation Higashi et al, 2000;Cantuaria et al, 2001). GLUT1 expression in tumors also correlates with the survival of patients.…”

Section: Glut Expression In Tumorsmentioning

confidence: 99%

Molecular and cellular regulation of glucose transporter (GLUT) proteins in cancer

Macheda

Rogers

Best

2004

Journal Cellular Physiology

1,035

893

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“…Determination of malignant lesions with PET/CT is based on their glucose metabolism [20,21]. The overexpression of Glut1 is closely related to FDG uptake in human cancer [20,21]. Glut1 is thought to be a possible intrinsic marker of hypoxia, and its expression is regulated by hypoxia via HIF-1 [22,23].…”

Section: Discussionmentioning

confidence: 99%

“…HIF-1a protein is specifically induced by hypoxia in a graded response dependent on the oxygen concentration [5]. Determination of malignant lesions with PET/CT is based on their glucose metabolism [20,21]. The overexpression of Glut1 is closely related to FDG uptake in human cancer [20,21].…”

Section: Discussionmentioning

confidence: 99%

Correlation of hypoxia inducible transcription factor in breast cancer and SUVmax of F-18 FDG PET/CT

Jeong

Jung

Cho³

et al. 2017

Nucl. Med. Rev.

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“…Several studies have shown that high glucose uptake or Glut-1 expression predicts poor prognosis and that Glut-1 levels often are elevated in 18F-FDG-avid tumors, [30][31][32][33][34][35][36][37][38][39][40][41] but their regional or microregional spatial association has seldom been studied and remains unclear. Our colocalization analysis of 18 F-FDG uptake and Glut-1 expression shows some, albeit weak, spatial linkage and again the strongest correlation was observed in the relatively nonglycolytic tumor model (Table I).…”

Section: Discussionmentioning

confidence: 99%

Aerobic glycolysis in cancers: Implications for the usability of oxygen‐responsive genes and fluorodeoxyglucose‐PET as markers of tissue hypoxia

Busk

Horsman

Kristjansen

et al. 2008

Intl Journal of Cancer

105

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The hypoxia-responsiveness of the glycolytic machinery may allow pretreatment identification of hypoxic tumors from HIF-1 targets (e.g., Glut-1) or [18F]-fluorodeoxyglucose positron emission tomography but results have been mixed. We hypothesized that this discrepancy is an inevitable consequence of elevated aerobic glycolysis in tumors (Warburg effect) as energetics in predominantly glycolytic cells is little affected by hypoxia. Accordingly, we characterized glycolytic and mitochondrial ATP generation in normoxic and anoxic cell lines. Measurements demonstrated that most cancer cells rely largely on aerobic glycolysis as it accounts for 56-63% of their ATP budget, but in the cervical carcinoma SiHa, ATP synthesis was mainly mitochondrial. Moreover, the stimulatory effect of anoxia on glycolytic flux was inversely correlated to the relative reliance on aerobic glycolysis. Next, tumor cells representing a Warburg or a nonglycolytic phenotype were grown in mice and spatial patterns of hypoxia (pimonidazolestained), Glut-1 expression and 18 F-FDG uptake were analysed on sectioned tumors. Only in SiHa tumors did foci of elevated glucose metabolism consistently colocalize with regions of hypoxia and elevated Glut-1 expression. In contrast, spatial patterns of Glut-1 and pimonidazole staining correlated reasonably well in all tumors. In conclusion, Glut-1's value as a hypoxia marker is not severely restricted by aerobic glycolysis. In contrast, the specificity of 18 F-FDG uptake and Glut-1 expression as markers of regional hypoxia and glucose metabolism, respectively, scales inversely with the intensity of the Warburg effect. This linkage suggests that multi-tracer imaging combining FDG and hypoxia-specific markers may provide therapeutically relevant information on tumor energetic phenotypes. ' 2008 Wiley-Liss, Inc.Key words: hypoxia; Warburg; Pasteur; fluorodeoxyglucose; Glut-1 German biologist Otto Warburg 1 changed our understanding of tumor energy metabolism, by demonstrating that cancer cells deviate from their nontransformed counterparts by a vigorous formation of lactate even in the presence of oxygen (i.e., aerobic glycolysis). Mitochondrial defects are widespread in cancers and Warburg rationally hypothesized that impaired respiratory capacity leads to a compensatory increase in glycolysis. However, the cause and effect relationship between the oxidative phosphorylation (OXPHOS) and aerobic glycolysis is unclear, as at least some cancer cell lines are able to increase oxygen consumption rate (OCR) when glycolysis is inhibited or when treated with mitochondrial uncouplers. 2,3 Cancer cell energy metabolism has received renewed interest recently, when some common oncogenic mutations have been directly linked to the glycolytic phenotype, 4,5 but tumor hypoxia is common, and the imposed ATP deficit could be an important trigger of high glucose consumption in vivo (Pasteur effect).Tumor hypoxia, in particular in squamous cell carcinomas (SCCs), adversely affects prognosis by enhancing resistance to radio-and ch...

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Correlation of Glut-1 glucose transporter expression with [18F]FDG uptake in non-small cell lung cancer

Cited by 179 publications

References 14 publications

Molecular and cellular regulation of glucose transporter (GLUT) proteins in cancer

Molecular and cellular regulation of glucose transporter (GLUT) proteins in cancer

Correlation of hypoxia inducible transcription factor in breast cancer and SUVmax of F-18 FDG PET/CT

Aerobic glycolysis in cancers: Implications for the usability of oxygen‐responsive genes and fluorodeoxyglucose‐PET as markers of tissue hypoxia

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