Abstract
Autophagy is a central process in regulation of cell survival, cell death and proliferation and plays an important role in carcinogenesis, including thyroid carcinoma. Genetic variation in autophagy components has been demonstrated to influence the capacity to execute autophagy and is associated with disease susceptibility, progression and outcome. In the present study, we assessed whether genetic variation in autophagy genes contributes to susceptibility to develop thyroid carcinoma, disease progression and/or patient outcome. The results indicate that patients carrying the ATG5 single nucleotide polymorphisms rs2245214 have a higher probability to develop thyroid carcinoma (OR 1.85 (95% CI 1.04–3.23), P = 0.042). In contrast, no significant differences could be observed for the other genetic variants studied in terms of thyroid carcinoma susceptibility. Furthermore, none of the selected genetic variants were associated with clinical parameters of disease progression and outcome. In conclusion, genetic variation in ATG5, a central player in the autophagy process, is found to be associated with increased susceptibility for thyroid carcinoma, indicating a role for autophagy in thyroid carcinogenesis.
Highlights
Epithelial cell derived non-medullary thyroid cancer (NMTC) is the most common endocrine malignancy with a rising incidence during the last decades of which papillary thyroid carcinoma (PTC) and follicular thyroid carcinoma (FTC) represent the vast majority of cases [1,2,3]
The present study was performed to investigate whether common genetic variants in human autophagy genes are associated with NMTC susceptibility, severity and/or clinical outcome
We found that one of the selected genetic variants, the ATG5 rs2245214 single nucleotide polymorphism, is significantly associated with NMTC susceptibility, but not with NMTC severity or outcome
Summary
Epithelial cell derived non-medullary thyroid cancer (NMTC) is the most common endocrine malignancy with a rising incidence during the last decades of which papillary thyroid carcinoma (PTC) and follicular thyroid carcinoma (FTC) represent the vast majority of cases [1,2,3]. An autophagosome is formed which engulfs cellular components such as organelles, ribosomes and protein aggregates, which are subsequently degraded by fusion of the autophagosome with a lysosome. Autophagy has an important role in the regulation of cell death, cell differentiation, induction of cell cycle arrest, and modulation of inflammation [8]. Autophagy may have both preventive and promotional effects on tumorigenesis, which is probably dependent on the type of autophagy initiation, tumor cell type and the stage of tumor development [9,10]. It is important to identify the mechanisms that regulate autophagy in malignant transformed cells
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