Overexpression of RYBP inhibits proliferation, invasion, and chemoresistance to cisplatin in anaplastic thyroid cancer cells via the EGFR pathway

• Published in: Journal of biochemical and molecular toxicology 2019-02, Vol.33 (2), p.e22241-n/a
• Main Authors: Tong, Ai‐Hua, Tan, Juan, Zhang, Jin‐Hua, Xu, Fang‐Jiang, Li, Fu‐Yuan, Cao, Chun‐Yu
• Format: Article
• Language: English
• Subjects: anaplastic thyroid cancer (ATC); Biological activity; Cancer; Cell Line, Tumor; Cell proliferation; Cell Proliferation - drug effects; Cell Proliferation - genetics; Chemoresistance; Chemotherapy; Cisplatin; Cisplatin - pharmacology; Drug Resistance, Neoplasm - drug effects; Drug Resistance, Neoplasm - genetics; Epidermal growth factor receptors; Humans; Intracellular Signaling Peptides and Proteins - biosynthesis; Intracellular Signaling Peptides and Proteins - genetics; invasion; MAP Kinase Signaling System - drug effects; MAP Kinase Signaling System - genetics; Neoplasm Invasiveness; Neoplasm Proteins - biosynthesis; Neoplasm Proteins - genetics; Phosphorylation; Polycomb group proteins; proliferation; Proteins; Ring1 and YY1 binding protein (RYBP); Therapeutic applications; Thyroid; Thyroid cancer; Thyroid Carcinoma, Anaplastic - drug therapy; Thyroid Carcinoma, Anaplastic - genetics; Thyroid Carcinoma, Anaplastic - metabolism; Thyroid Carcinoma, Anaplastic - pathology; Thyroid Neoplasms - drug therapy; Thyroid Neoplasms - genetics; Thyroid Neoplasms - metabolism; Thyroid Neoplasms - pathology; YY1 protein
• ISSN: 1095-6670; 1099-0461
• DOI: 10.1002/jbt.22241

Ring1 and YY1 binding protein (RYBP), a new member of the polycomb group protein family, has been reported to play an important role in various biological processes. Recently, more and more studies have demonstrated an implication of RYBP in cancer development. However, the specific role of RYBP in anaplastic thyroid cancer (ATC) remains unknown. In this study, we investigated for the first time the expression pattern and biological functions of RYBP in ATC. We showed that RYBP was lowly expressed in ATC tissues and cell lines. We also found that overexpression of RYBP inhibited ATC cell proliferation, invasion, and cisplatin resistance. Furthermore, we observed that upregulation of RYBP decreased the phosphorylation of EGFR and ERK1/2 in ATC cells. Taken together, our data indicated that RYBP might be considered as a promising therapeutic target for the treatment of ATC.