CITED1 contributes to the progression of papillary thyroid carcinoma via the Wnt/β-catenin signaling pathway.

Abstract

PurposeThe incidence rate of thyroid cancer, the most common endocrine malignancy, has increased rapidly over the past 10 years. However, the fundamental molecular mechanisms underlying the malignant progression of thyroid cancer are unclear.Materials and methodsFirstly, quantitative real-time PCR analysis and Western blot analysis were used to investigate the expression of Cbp/p300 interacting transactivator with Glu/Asp rich carboxy-terminal domain 1 (CITED1) in papillary thyroid carcinoma (PTC) cell lines. Then, we investigated the effects of CITED1 knockdown on cell proliferation, apoptosis, and invasion in in vitro and in vivo models of PTC.ResultsCITED1 was upregulated in PTC cell lines, and CITED1 knockdown significantly suppressed the proliferation, migration, and invasion of K1 cells resulting in a G0/G1 phase block. Furthermore, the silencing of CITED1 significantly promoted cell apoptosis. In the in vivo study, the growth speed and weight of the transplanted tumor were significantly suppressed in nude mice infected with short hairpin RNA targeting CITED1 (CITE1-shRNA) cells. Furthermore, we found that CITED1-shRNA activated Wnt/β-catenin signaling in PTC.ConclusionTaken together, our findings suggest that CITED1 knockdown facilitates apoptosis and inhibits proliferation and invasion in K1 cells via the Wnt/β-catenin signaling pathway.