Journal
ENDOCRINOLOGY AND METABOLISM
Volume 34, Issue 3, Pages 215-225Publisher
KOREAN ENDOCRINE SOC
DOI: 10.3803/EnM.2019.34.3.215
Keywords
Thyroid neoplasms; Sodium-iodide symporter; Isotopes
Categories
Funding
- National Natural Sciences Foundation of China [81771875, 81571714]
- Medicine and Technology Innovation Project of the Chinese Academy of Medical Science [2016-12M-2-006]
- Thyroid Study Group Project of the Asia Oceania Research Initiative Network (AORIN)
Ask authors/readers for more resources
The retained functionality of the sodium iodide symporter (NIS) expressed in differentiated thyroid cancer (DTC) cells allows the further utilization of post-surgical radioactive iodine (RAI) therapy, which is an effective treatment for reducing the risk of recurrence, and even the mortality, of DTC. Whereas, the dedifferentiation of DTC could influence the expression of functional NIS, thereby reducing the efficacy of RAI therapy in advanced DTC. Genetic alternations (such as BRAF and the rearranged during transfection [RET]/papillary thyroid cancer [PTC] rearrangement) have been widely reported to be prominently responsible for the onset, progression, and dedifferentiation of PTC, mainly through activating the mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K) signaling cascades. These genetic alternations have been suggested to associate with the reduced expression of iodide-handling genes in thyroid cancer, especially the NIS gene, disabling iodine uptake and causing resistance to RAI therapy. Recently, novel and promising approaches aiming at various targets have been attempted to restore the expression of these iodine-metabolizing genes and enhance iodine uptake through in vitro studies and studies of RAI-refractory (RAIR)-DTC patients. In this review, we discuss the regulation of NIS, known mechanisms of dedifferentiation including the MAPK and PI3K pathways, and the current status of redifferentiation therapy for RAIR-DTC patients.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available