Abstract
Radiation-induced damage is a complex network of interlinked signaling pathways, which may result in apoptosis, cell cycle arrest, DNA repair, and cancer. The development of thyroid cancer in response to radiation, from nuclear catastrophes to chemotherapy, has long been an object of study. A basic overview of the ionizing and non-ionizing radiation effects of the sensitivity of the thyroid gland on radiation and cancer development has been provided. In this review, we focus our attention on experiments in cell cultures exposed to ionizing radiation, ultraviolet light, and proton beams. Studies on the involvement of specific genes, proteins, and lipids are also reported. This review also describes how lipids are regulated in response to the radiation-induced damage and how they are involved in thyroid cancer etiology, invasion, and migration and how they can be used as both diagnostic markers and drug targets.
Highlights
Radiation includes ionizing radiation (IR) and non-IR
The study of the survivors in Hiroshima and Nagasaki has demonstrated that the risk for thyroid cancer was significantly higher if IR exposure occurred at pediatric ages [9]
Richardson [14] stated that exposure to IR in adulthood was positively associated with thyroid cancer among female survivors from atomic bombs (excess relative rate/Gray (Gy) = 0.70; 90% confidence interval = 0.20–1.46), the risk seemed to be lower if they were exposed to radiation in their childhood
Summary
Radiation includes ionizing radiation (IR) and non-IR. The acute radiation syndrome is caused by the exposure to high IR during a short period of time, causing depletion of parenchymal cells in a tissue [2]. The chronic radiation syndrome, ranging from dose-limiting toxicity to the increased risk of secondary cancers following radiation in patients, should always be considered [5]. To this end, adaptive responses to low radiation doses have been widely studied both in vitro and in vivo to ascertain the biological mechanism of radiation action. Radiation-induced signaling pathways in different tissues via EGFR, IGFI-R, PI3K, MAPK, JNK, and p38, as well as via FAS-R, TNF-R, and NFKB, have been reviewed [6]
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