Thyroid cancer (TC) is one of the most common malignancies with a high mortality rate. Long non-coding RNA CCAT2 (CCAT2) participates in the occurrence and development of certain human cancers; however, whether it is involved in TC remains unclear. Thus, the present study investigated the role of CCAT2 in TC and the underlying mechanism. CCAT2 expression in both TC tissues and cell lines was examined by reverse transcription-quantitative PCR. CCAT2 expression was silenced in TC cell lines by a specific small interfering (si)RNA against CCAT2 (si-CCAT2). The effects of CCAT2 silencing on TC cell proliferation were detected by CCK-8 and colony formation assays. Cell cycle and apoptosis of the treated TC cells were assessed by flow cytometry. Wound healing and Transwell assays were performed to detect the effects of si-CCAT2 on the migration and invasion of TC cells. Apoptosis-related proteins and Wnt/β-catenin cascade-associated agents were examined by western blotting. The interaction between CCAT2 and the Wnt/β-catenin pathway in the transfected cells was detected by performing a dual-luciferase reporter assay. CCAT2 expression was increased in TC tissue samples and cell lines compared with the controls. Tissue CCAT2 level was associated with T stage and tumor-node-metastasis stage of TC. Silencing CCAT2 inhibited TC cell proliferation, migration and invasion, and promoted TC cell cycle arrest and apoptosis. Furthermore, CCAT2 knockdown suppressed the activity of the Wnt/β-catenin cascade in TC cells treated with lithium chloride. In summary, the present study demonstrated that CCAT2 knockdown suppresses TC progression via inactivating the Wnt/β-catenin cascade, indicating that suppressing CCAT2 and the Wnt/β-catenin signaling pathway may be a promising therapeutic strategy for treating TC.

Diabetes mellitus (DM) is a kind of metabolic disorder characterized by long-term hyperglycemia. Oxidative stress is involved in inducing the apoptosis of pancreatic β-cells and promoting the development of DM. Oxalomalate (OMA) is a competitive inhibitor of two classes of NADP+-dependent isocitrate dehydrogenase isoenzymes that are the main nicotinamide adenine dinucleotide phosphate (NADPH) producers to scavenge cellular reactive oxygen species (ROS). However, the role of OMA in DM remains unclear. The present study aimed to investigate the protective effects of OMA on streptozotocin (STZ)-induced β-cell damage and its underlying mechanisms. The viability of rat insulinoma cell line (INS-1) and the contents of ROS, nitric oxide and NAPDH were examined after cells being treated with STZ. After treatment with OMA in STZ-stimulated INS-1, the cell viability, apoptosis, and apoptosis-related proteins were measured. Meanwhile, the levels of oxidative stress-related factors and the changes of insulin secretion were determined. The results revealed that OMA significantly increased the cell viability (p < .05), reduced the apoptotic rate (p < .001), and altered the expression levels of Bcl-2, Bax, cleaved caspase3, and cleaved-caspase9 (p < .05 or p < .01) in STZ-induced INS-1 cells. Moreover, OMA enhanced the activities of superoxide dismutase, catalase, glutathione peroxidase (p < .01), whereas reduced the levels of ROS, malondialdehyde and lactic dehydrogenase (p < .001). Furthermore, OMA improved the ability of insulin secretion. These results indicated that OMA might have antioxidative stress and anti-apoptosis effects to protect INS-1 cells from STZ-induced cell damage. K E Y W O R D S cell apoptosis, diabetes mellitus, Oxalomalate, oxidative stress, reactive oxygen species