Abstract
PurposeThis study aimed to investigate the expression of glutamine metabolism-related protein in tumor and stromal compartments among the histologic subtypes of thyroid cancer.ResultsGLS1 and GDH expression in tumor and stromal compartments were the highest in AC than in other subtypes. Tumoral ASCT2 expression was higher in MC but lower in FC (p < 0.001). In PTC, tumoral GLS1 and tumoral GDH expression was higher in the conventional type than in the follicular variant (p = 0.043 and 0.001, respectively), and in PTC with BRAF V600E mutation than in PTC without BRAF V600E mutation (p<0.001). Stromal GDH positivity was the independent factor associated with short overall survival (hazard ratio: 21.48, 95% confidence interval: 2.178-211.8, p = 0.009).MethodsWe performed tissue microarrays with 557 thyroid cancer cases (papillary thyroid carcinoma [PTC]: 344, follicular carcinoma [FC]: 112, medullary carcinoma [MC]: 70, poorly differentiated carcinoma [PDC]: 23, and anaplastic carcinoma [AC]: 8) and 152 follicular adenoma (FA) cases. We performed immunohistochemical staining of glutaminolysis-related proteins (glutaminase 1 [GLS1], glutamate dehydrogenase [GDH], and amino acid transporter-2 [ASCT-2]).ConclusionGlutamine metabolism-related protein expression differed among the histologic subtypes of thyroid cancer.
Highlights
We aimed to investigate the metabolism in thyroid cancer, especially glutamine metabolism in this study
Glutamine metabolism-related protein expression differed among the histologic subtypes of thyroid cancer
It was reported that ammonia, which is produced by tumor cell glutaminolysis migrates into the stroma, leading to increased autophagy of stromal cells
Summary
We aimed to investigate the metabolism in thyroid cancer, especially glutamine metabolism in this study. Glutamine metabolism is a critical pathway in cancer cell metabolism [2]. Cancer cells have been shown to metabolize glutamine more than other amino acids [3, 4]. In glutamine metabolic pathway, the interaction between cancer cells and stromal cells is present. It was reported that ammonia, which is produced by tumor cell glutaminolysis migrates into the stroma, leading to increased autophagy of stromal cells. Glutamine was reported to be produced as the product of autophagy activity, travel back to tumor cells and utilized in glutamine metabolism [5,6,7,8,9]
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