Abstract
Thyroid hormone receptor-interacting protein 6 (TRIP6), a member of the zyxin family of Lin-Isl-Mec (LIM) proteins, is an adaptor protein primarily expressed in epithelial cells. TRIP6 can regulate a variety of cellular responses, such as actin cytoskeletal reorganization and cell adhesion. However, to the best of our knowledge, the role of TRIP6 in osteosarcoma (Os) has not been previously reported. Therefore, the present study investigated the role of TRIP6 in the occurrence and development of Os, and the potential of utilizing TRIP6 as a therapeutic target in Os. The present results suggested that the expression levels of TRIP6 were significantly increased in Os cells and clinical tissue specimens compared with normal osteoblasts and adjacent non-tumor tissue. Moreover, the present results suggested that overexpressing TRIP6 significantly increased proliferation, migration and invasion, while inhibiting apoptosis in Os cells. However, silencing TRIP6 decreased proliferation, migration and invasion, while activating apoptosis in Os cells. The present results suggested that overexpression of TRIP6 increased NF-κB activation by decreasing the protein expression levels of inhibitor of κBα, and increasing total and phosphorylated P65 levels. The present results indicated that TRIP6 silencing decreased NF-κB activation. Collectively, the present results suggested that TRIP6 may play a role in promoting Os cell proliferation, migration and invasion, while inhibiting cell apoptosis. Furthermore, TRIP6 may be utilized as a novel prognostic biomarker and therapeutic target in Os.