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A vast amount of evidence indicates that long non-coding RNAs (lncRNAs) are involved in cancer. Previous studies have indicated that lncRNA DiGeorge syndrome critical region gene 5 (DGCR5) is aberrantly expressed in lung cancer, pancreatic ductal adenocarcinoma and hepatocellular carcinoma. However, the role of DGCR5 in papillary thyroid carcinoma (PTC) has remained elusive. In the present study, it was revealed that DGCR5 was significantly downregulated in PTC tissues compared with that in adjacent normal tissues. Through functional experiments, it was demonstrated that ectopic overexpression of DGCR5 markedly suppressed PTC cell growth and invasion. A bioinformatics analysis suggested that DGCR5 binds to microRNA (miR)-2861. A total of 5 putative binding sites for miR-2861 were identified in DGCR5, and a luciferase reporter assay confirmed the direct interaction between DGCR5 and miR-2861. Furthermore, reverse transcription-quantitative polymerase chain reaction analysis indicated that ectopic overexpression of DGCR5 led to a decreased expression of miR-2861 in PTC cells and miR-2861 mimic transfection caused a downregulation of DGCR5. miR-2861 level was upregulated in PTC tissues compared with adjacent tissues and negatively correlated with DGCR5 level. In addition, rescue experiments indicated that ectopic expression of miR-2861 reversed the effects of DGCR5 overexpression on PTC cell proliferation and invasion. Taken together, the present results demonstrated that DGCR5 inhibits PTC progression via sponging miR-2861, indicating DGCR5 may serve as a therapeutic target. [ABSTRACT FROM AUTHOR]

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 factor‑κB (NF‑κB) was associated with resistance to 131I in cancer cells. The present study aimed to investigate the effects of NF‑κB on 131I 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 131I 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 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 NF‑κB 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 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 131I uptake of thyroid cancer cells, this inhibition may increase the apoptotic effects of radioactive 131I. [ABSTRACT FROM AUTHOR]