OVEREXPRESSION OF CASEIN KINASE 1 EPSILON AS A THERAPEUTIC TARGET IN THYROID CANCER

AUTHORS:
S. Cheng (Taipei, Taiwan) , C. Kuo (Taipei, Taiwan) , C. Tsai (Taipei, Taiwan) , M. Chien (Taipei, Taiwan)
Background:
An integrated microarray analysis identified casein kinase 1 epsilon (CSNK1E) as one of the circadian rhythm genes driving anaplastic thyroid cancer progression. The casein kinase I family of serine/threonine protein kinases is implicated in the transcription-translation feedback loops; however, the functional roles of CSNK1E in thyroid cancer remain unknown.
Methods:
Protein expression of CSNK1E in benign and malignant thyroid neoplasms was evaluated using immunohistochemical staining. Thyroid cancer cell lines were treated with CSNK1E inhibitors PF670462 and IC261 and subjected to various assays.
Results:
Compared to normal thyroid tissue or follicular adenoma, CSNK1E was overexpressed in differentiated and undifferentiated thyroid cancers. Following treatment with CSNK1E inhibitors, cell viability was suppressed, accompanied by arrest of cell cycle progression and cyclin D1 downregulation. Additionally, CSNK1E inhibitors decreased cell migration and invasion and attenuated expression of epithelial-mesenchymal transition markers.
Conclusions:
Thyroid cancer exhibits aberrant CSNK1E expression, and targeting CSNK1E holds promising therapeutic potential.