CHI3L1 Inhibits Expression of NIS by Activating MEK/ERK1/2 Signal Pathway in Thyroid Cancer

Abstract

Purpose To study the differentially expressed protein between thyroid cancer and radioactive iodine refractory differentiated thyroid cancer (RR-DTC), which presents highly aggressive and unfavorable prognosis. Meanwhile, to search for a potential radiotherapeutic target for patients suffer from RR-DTC. Methods Totally 6 metastatic lymph nodes of RR-DTC and DTC were collected during lymph node dissection for proteomics studies. Immunohistochemical staining was performed to verify the expression of Chitinase-3-like 1 (CHI3L1) in RR-DTC and DTC tissues. Western blotting was used to detect the expression of sodium-iodine symporter (NIS), MEK, and ERK1/2 in CHI3L1 over-expression stable transfectants, control stable transfectants, and PTC-K1 cells. Results CHI3L1 was demonstrated to be significantly up-regulated in RR-DTC by immunohistochemical staining. Besides, CHI3L1 over expression would inhibit expression of sodium-iodine symporter, a key protein for iodine accumulation, by activating MEK/ERK1/2 signal pathway. Conclusion CHI3L1 might be a potential molecular target for RR-DTC due to its over expression in RR-DTC and membrane location.