ICT1 Knockdown inhibits osteosarcoma cell proliferation by regulating cell apoptosis through targeting BCL-2

Background:Osteosarcoma (OS) which occurs mainly in the young people is a familiar malignant bone tumor. Apoptosis is a kind of programmed and managed cell death and promoting apoptosis of OS cells is an important treatment for OS. However, the pathways of controlling apoptosis in OS remain unclear. Immature colon carcinoma transcript-1 (ICT1) belongs to a family of four putative mitochondrial translation release factors. It controls the termination stage of translation. Methods:In this study, the function of ICT1 was elucidated by a series of in vivo and in vitro assays. The potential downstream targets of ICT1 in the OS was confirmed by Quantitative real‑time polymerase chain reaction (qRT-PCR) and western blotting, while immunohistochemical analysis and rescue experiment were performed to confirm this result. Results: ICT1 was significantly upregulated in osteosarcoma, and higher expression of ICT1 led to the worse survival rate. Furthermore, knockdown of ICT1 could inhibit the cell proliferation, but improved the apoptosis of cells in vitro and in vivo. In addition, our data demonstrated that BCL-2, apoptotic related-genes, is a potential target of ICT1 and the overexpression of BCL-2 partly reduced the negative influence of ICT1 knockdown on the pro-tumorigenic capabilities of OS cells in vitro. Conclusion: The ICT1 protein was overexpressed in the OS and has identified a novel mechanism by which ICT1 inhibits osteosarcoma cell proliferation by regulating cell apoptosis through targeting BCL-2.