Effects of nuclear factor-κB on the uptake of (131)iodine and apoptosis of thyroid carcinoma cells

Thyroid carcinoma is primarily treated by surgery combined with radioactive (131)iodine ((131)I) treatment; however, certain patients exhibit resistance to (131)I treatment. Previous research indicated that nuclear factor-κB (NF-κB) was associated with resistance to (131)I in cancer cells. The present study aimed to investigate the effects of NF-κB on (131)I uptake and apoptosis in thyroid carcinoma cells. TPC-1 and BCPAP cell lines were employed as research models in the present study, and the expression of NF-κB was inhibited by RNA interference (RNAi). The ability of TPC-1 and BCPAP cells to uptake (131)I was measured and the cell viability was detected by an MTT assay. Finally, the expression of the apoptosis-associated proteins X-linked inhibitor of apoptosis (XIAP), cellular inhibitor of apoptosis protein 1 (cIAP1) and caspase-3 in TCP-1 and BCPAP cells was determined by western blotting. Western blotting results demonstrated that the expression levels of NF-κB in TPC-1 and BCPAP cells were successfully downregulated by RNAi (P<0.05), while analysis of (131)I uptake revealed no significant alterations in the (131)I uptake ability of cells following RNAi (P>0.05). MTT experiments demonstrated that the inhibition of NF-κB expression in combination with radiation ((131)I treatment) led to a marked reduction in cell viability (P<0.05). Furthermore, western blot analysis revealed that the inhibition of NF-κB expression downregulated the expression levels of XIAP and cIAP1 (P<0.05), while the expression levels of caspase-3 were upregulated, indicating that the observed reduction in cell viability following NF-κB inhibition may be due to an increased level of apoptosis. Although NF-κB inhibition did not affect the (131)I uptake of thyroid cancer cells, this inhibition may increase the apoptotic effects of radioactive (131)I.