Thyroid carcinoma is primarily treated by surgery combined with radioactive 131iodine (131I) treatment; however, certain patients exhibit resistance to 131I treatment. Previous research indicated that nuclear factorkappaB (NFkappaB) was associated with resistance to 131I in cancer cells. The present study aimed to investigate the effects of NFkappaB on 131I uptake and apoptosis in thyroid carcinoma cells. TPC1 and BCPAP cell lines were employed as research models in the present study, and the expression of NFkappaB was inhibited by RNA interference (RNAi). The ability of TPC1 and BCPAP cells to uptake 131I was measured and the cell viability was detected by an MTT assay. Finally, the expression of the apoptosisassociated proteins Xlinked inhibitor of apoptosis (XIAP), cellular inhibitor of apoptosis protein 1 (cIAP1) and caspase3 in TCP1 and BCPAP cells was determined by western blotting. Western blotting results demonstrated that the expression levels of NFkappaB in TPC1 and BCPAP cells were successfully downregulated by RNAi (P<0.05), while analysis of 131I uptake revealed no significant alterations in the 131I uptake ability of cells following RNAi (P>0.05). MTT experiments demonstrated that the inhibition of NFkappaB expression in combination with radiation (131I treatment) led to a marked reduction in cell viability (P<0.05). Furthermore, western blot analysis revealed that the inhibition of NFkappaB expression downregulated the expression levels of XIAP and cIAP1 (P<0.05), while the expression levels of caspase3 were upregulated, indicating that the observed reduction in cell viability following NFkappaB inhibition may be due to an increased level of apoptosis. Although NFkappaB inhibition did not affect the 131I uptake of thyroid cancer cells, this inhibition may increase the apoptotic effects of radioactive 131I.