Effect to Therapy of Sodium-Iodine Symporter Expression by Alpha-Ray Therapeutic Agent via Sodium/Iodine Symporter

This study confirmed the effect of sodium/iodine symporter (NIS) expression on existing drugs by in vitro and in vivo tests using cultured cell lines. The tumor growth inhibitory effect of sodium astatide ([At-211]NaAt) was evaluated by in vitro and in vivo tests using human thyroid cancer cells (K1, K1/NIS and K1/NIS-DOX). NIS expression in cancer cells was controlled using the Tet-On system. [I-131]NaI was used as control existing drug. From the results of the in vitro studies, the mechanism of [At-211]NaAt uptake into thyroid cancer cells is mediated by NIS, analogous to [I-131]NaI, and the cellular uptake rate correlates with the expression level of NIS. [At-211]NaAt's ability to inhibit colony formation was more than 10 times that of [I-131]NaI per becquerel (Bq), and [At-211]NaAt's DNA double-strand breaking (DSB) induction was more than ten times that of [I-131]NaI per Bq, and [At-211]NaAt was more than three times more cytotoxic than [I-131]NaI (at 1000 kBq each). In vivo studies also showed that the tumor growth inhibitory effect of [At-211]NaAt depended on NIS expression and was more than six times that of [I-131]NaI per Bq.

Automated summary

This study confirmed the impact of sodium/iodine symporter (NIS) expression on existing drugs through in vitro and in vivo tests. The results showed that sodium astatide ([At-211]NaAt) had a stronger tumor growth inhibitory effect compared to sodium iodide ([I-131]NaI), and the uptake rate correlated with NIS expression.