lncRNA CASC2 Enhances (131)I Sensitivity in Papillary Thyroid Cancer by Sponging miR-155

Long noncoding RNA cancer susceptibility candidate 2 (CASC2) has been reported to play an anticancer role in papillary thyroid cancer (PTC). Radioiodine ((131)I) is a common option for the treatment of PTC. However, the role and mechanism of CASC2 in (131)I sensitivity remain unclear. In this study, (131)I-resistant cells were constructed through continuous treatment of (131)I. The expression levels of CASC2 and miR-155 were measured by qRT-PCR. The IC50 of (131)I was analyzed by cell viability using MTT assay. Flow cytometry was conducted to determine cell apoptosis induced by (131)I. The association between CASC2 and miR-155 was evaluated by luciferase assay and RNA immunoprecipitation. A mouse xenograft model was built to explore the effect of CASC2 on the growth of (131)I-resistant PTC cells in vivo. Results showed that CASC2 expression was decreased in PTC tissues and cells, and low expression of CASC2 was associated with poor outcome of patients. CASC2 level was reduced in (131)I-resistant cells. Knockdown of CASC2 inhibited (131)I sensitivity in thyroid cancer cells. Overexpression of CASC2 enhanced (131)I sensitivity in constructed resistant PTC cells. CASC2 was a decoy of miR-155, and CASC2-mediated promotion of (131)I sensitivity was weakened by decreasing miR-155. Abundance of CASC2 inhibited the growth of (131)I-resistant cells in vivo. As a conclusion, CASC2 increases (131)I sensitivity in PTC by sponging miR-155, providing a novel target for the treatment of thyroid cancer patients with (131)I resistance.