RBBP6 promotes human cervical carcinoma malignancy via JNK signaling pathway

Abstract

Previous studies have shown that retinoblastoma binding protein 6 (RBBP6) was overexpressed in malignant tumors and was correlated with poorer prognosis in various cancers. However, its role in cervical carcinoma has not been elucidated. This study was to investigate the relationship between RBBP6 and cervical carcinoma. Cervical carcinoma cell lines SiHa and C33a were used to assess the effect of RBBP6 on cell viability, migration, and proliferation. RBBP6 mRNA and protein levels in cervical cancer tissues increased at least three times as that in the adjacent non-cancerous tissues. Overexpression of RBBP6 in SiHa and C33a cell lines resulted in increased phosphorylated c-Jun NH2-terminal kinase (p-JNK) as well as increased cell viability, migration, and proliferation. Moreover, this effect was suppressed by specific JNK inhibitor SP600125. RBBP6 might potentiate cervical carcinoma cell viability, migration and proliferation through JNK signaling pathway. RBBP6 and JNK inhibitor may be beneficial as a novel preventive and therapeutic target for cervical cancer.