Knockdown of EIF3C promotes human U-2OS cells apoptosis through increased CASP3/7 and Chk1/2 by upregulating SAPK/JNK

As a component of the EIF3 complex, EIF3C is essential for several steps in protein synthesis initiation. Recently, it has been addressed that EIF3C is overexpressed in several human cancers and plays a pivotal role in cell proliferation and tumorigenesis.

Immunohistochemistry, quantitative real-time PCR (qPCR), and Western blotting assays were employed to determine the expression of EIF3C in osteosarcoma (OsC) tissues obtained from 60 patients. The levels of EIF3C mRNA and protein were assessed by qPCR and Western blotting, respectively. The effect of EIF3C knockdown on OsC cell proliferation was detected by MTT and colony formation assays, respectively. Cell apoptosis induced by EIF3C silencing was analyzed by flow cytometric analysis. PathScan stress and apoptosis signaling antibody array kit was used to analyze the potential effects of EIF3C knockdown on OsC cells.

The levels of EIF3C were high in OsC tissues and cell lines. In addition, EIF3C knockdown by lentivirus-mediated shRNA targeting EIF3C significantly suppressed cell proliferation and colony formation and induced apoptosis in U-2OS cells. Moreover, EIF3C knockdown led to the upregulated expression of CASP3/7, Chk1/2, and SAPK/JNK, indicating that the downregulated expression of EIF3C might be associated with pro-apoptosis of U-2OS cells.

EIF3C may be a promising target for gene therapy of human OsC. However, the precise mechanisms behind the effect of EIF3C on OsC tumorigenesis require further analysis.