TIGAR Is Correlated with Maximal Standardized Uptake Value on FDG-PET and Survival in Non-Small Cell Lung Cancer

Zhou, Xiang; Xie, Wenhui; Li, Qian; Zhang, Yifan; Zhang, Jie; Zhao, Xiaoping; Liu, Jianjun; Huang, Gang

doi:10.1371/journal.pone.0080576

Cited by 19 publications

(19 citation statements)

References 23 publications

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“…Total RNA was extracted from cells and tissues, and the extracted RNA was reverse transcribed and amplified by qRT-PCR as previously described22. The mRNA levels of the target genes were normalized to GAPDH.…”

Section: Methodsmentioning

confidence: 99%

IL-17 Promotes Angiogenic Factors IL-6, IL-8, and Vegf Production via Stat1 in Lung Adenocarcinoma

Huang

Duan

Qian

et al. 2016

Sci Rep

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Inflammation and angiogenesis are two hallmarks of carcinoma. The proinflammatory cytokine interleukin-17 (IL-17) facilitates angiogenesis in lung cancer; however, the underlying mechanism is not fully understood. In this study, tumour microvessel density (MVD) was positively associated with IL-17, interleukin-6 (IL-6), interleukin-8 (IL-8), and vascular endothelial cell growth factor (VEGF) expression in human lung adenocarcinoma tissues, and it was increased in tumour tissues of A549-IL-17 cell-bearing nude mice. Importantly, positive correlations were also detected between IL-17 expression and IL-6, IL-8 and VEGF expression in human lung adenocarcinoma tissues. Furthermore, IL-6, IL-8 and VEGF production, as well as STAT1 phosphorylation, were increased in tumour tissues of A549-IL-17 cell-bearing nude mice in vivo and in A549 and H292 cells following IL-17 stimulation in vitro. In addition, STAT1 knockdown using an inhibitor and siRNA attenuated the IL-17-mediated increases in IL-6, IL-8 and VEGF expression in A549 and H292 cells. In conclusion, IL-17 may promote the production of the angiogenic inducers IL-6, IL-8 and VEGF via STAT1 signalling in lung adenocarcinoma.

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Section: Methodsmentioning

confidence: 99%

IL-17 Promotes Angiogenic Factors IL-6, IL-8, and Vegf Production via Stat1 in Lung Adenocarcinoma

Huang

Duan

Qian

et al. 2016

Sci Rep

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“…Duan et al (26) reported that p53 expression is the primary predictive factor for SUV max . Zhou et al (27) found a significant difference between SUV max and Tp53-induced glycolysis and apoptosis regulator (TIGAR)’s being positive or negative. On the other hand, Watanabe et al (28) did not find a correlation between p53 alteration and FDG uptake.…”

Section: Discussionmentioning

confidence: 99%

The Diagnostic Value of the Correlation between Serum Anti-p53 Antibody and Positron Emission Tomography Parameters in Lung Cancer

Hasbek

Doǧan²,

Sarı³

et al. 2016

Mirt

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Objective:Mutations in the p53 gene are the most commonly observed genetic abnormalities in malignancies. The purpose of this study was to assess the diagnostic value of serum anti-p53 antibody (Ab) along with the correlation between serum anti-p53 Ab level and quantitative positron emission tomography (PET) parameters such as maximum standardized uptake value (SUVmax), SUVave, metabolic tumor volume, total lesion glycolysis (TLG) and tumor size.Methods:Serum anti-p53 Ab level was studied in three groups. Patients who underwent 18F-fluorodeoxyglucose (FDG) PET/computed tomography (CT) imaging for staging of previously diagnosed lung cancer constituted the first group, while patients who underwent 18F-FDG PET/CT imaging for evaluation of suspicious pulmonary nodules detected on thorax CT and did not show pathologic FDG accumulation (NAPN=pulmonary nodule with non avid-FDG) were enrolled in the second group. The third group consisted of healthy volunteers.Results:Twenty-eight patients with lung cancer (median age: 62.5, range: 39-77years), 28 patients with NAPN (median age: 65, range: 33-79 years), and 24 healthy volunteers (median age: 62, range: 44-74 years) were enrolled in the study. The serum anti-p53 Ab level was low in healthy volunteers while it was higher in both lung cancer patients and NAPN patients (p<0.05). When serum anti-p53 Ab level and PET parameters were evaluated, there was no significant correlation between serum anti-p53 Ab level and SUVmax, SUVave, TLG, tumor volume and tumor size of patients with lung cancer (p>0.05). Besides, there was no significant difference between serum anti-p53 Ab level and lesion size of NAPN patients (p>0.05).Conclusion:It was determined that serum anti-p53 Ab levels are not significantly correlated with PET parameters, and that serum anti-p53 Ab levels increase in any benign or malignant lung parenchyma pathology as compared to healthy volunteers. These results indicate that this Ab cannot be used as a predictor of malignancy in a lung lesion.

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“…This supports a two-compartment model of tumor metabolism. In vivo, TIGAR overexpression has been identified in several solid tumor types, including breast, glioblastoma, and non-small cell lung cancer, and in hematologic malignancies such as AML [66] [67] [68] [69]. TP53 mutations induce TIGAR expression more strongly than wild-type TP53 [63].…”

Section: Tigarmentioning

confidence: 99%

Metabolic coupling and the Reverse Warburg Effect in cancer: Implications for novel biomarker and anticancer agent development

Wilde

Roche

Domingo‐Vidal

et al. 2017

Seminars in Oncology

259

213

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Glucose is a key metabolite used by cancer cells to generate ATP, maintain redox state and create biomass. Glucose can be catabolized to lactate in the cytoplasm, which is termed glycolysis or alternatively can be catabolized to carbon dioxide and water in the mitochondria via oxidative phosphorylation (OXPHOS). Metabolic heterogeneity exists in a subset of human tumors, with some cells maintaining a glycolytic phenotype while others predominantly utilize OXPHOS. Cells within tumors interact metabolically with transfer of catabolites from supporting stromal cells to adjacent cancer cells. The Reverse Warburg Effect describes when glycolysis in the cancer-associated stroma metabolically supports adjacent cancer cells. This catabolite transfer, which induces stromal-cancer metabolic coupling, allows cancer cells to generate ATP, increase proliferation and reduce cell death. Catabolites implicated in metabolic coupling include the monocarboxylates lactate, pyruvate and ketone bodies. Monocarboxylate transporters (MCT) are critically necessary for release and uptake of these catabolites. MCT4 is involved in the release of monocarboxylates from cells, is regulated by catabolic transcription factors such as hypoxia inducible factor 1 alpha (HIF1A) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and is highly expressed in cancer-associated fibroblasts. Conversely, MCT1 is predominantly involved in the uptake of these catabolites and is highly expressed in a subgroup of cancer cells. MYC and TIGAR, which are genes involved in cellular proliferation and anabolism are inducers of MCT1. Profiling human tumors on the basis of an altered redox balance and intra-tumoral metabolic interactions may have important biomarker and therapeutic implications. Alterations in the redox state and mitochondrial function of cells can induce metabolic coupling. Hence, there is interest in redox and metabolic modulators as anticancer agents. Also, markers of metabolic coupling have been associated with poor outcomes in numerous human malignancies and may be useful prognostic and predictive biomarkers.

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TIGAR Is Correlated with Maximal Standardized Uptake Value on FDG-PET and Survival in Non-Small Cell Lung Cancer

Cited by 19 publications

References 23 publications

IL-17 Promotes Angiogenic Factors IL-6, IL-8, and Vegf Production via Stat1 in Lung Adenocarcinoma

IL-17 Promotes Angiogenic Factors IL-6, IL-8, and Vegf Production via Stat1 in Lung Adenocarcinoma

The Diagnostic Value of the Correlation between Serum Anti-p53 Antibody and Positron Emission Tomography Parameters in Lung Cancer

Metabolic coupling and the Reverse Warburg Effect in cancer: Implications for novel biomarker and anticancer agent development

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