Knockdown of eIF3a attenuated cell growth in K1 human thyroid cancer cells

Background In ribosome establishment and the initiation of translation, eukaryotic translation initiation factor (eIF) 3a is a pivotal functional subunit of the eIF3 complex. In various cancer types, abnormal eIF3a expression plays an important role in tumorigenesis. Objective We aimed to explore the role of eIF3a in human thyroid cancer (TC). Material and methods The expression of eIF3a was determined in TC tissues by qRT-PCR and immunohistochemistry (IHC) assay, respectively. In addition, the expression of eIF3a in K1 and BCPAP cells were detected by qRT-PCR. Cell proliferation, cell cycle, and cell apoptosis were assessed after eIF3a knockdown in K1 in cell line. Results The expression of eIF3a mRNA was high in TC tissues and cancer cell lines. Moreover, eIF3a expression in TC tissues indicated that high eIF3a level was associated with tumor grade. In addition, eIF3a knockdown resulted in a significantly decrease in cell proliferation and increased the apoptosis of K1 cells. Cell cycle was arrested in both the S and G2/M phase. The levels of phosphorylated ERK1/2 and surviving were decreased after eIF3a knockdown. Conclusion Our study suggested that eIF3a contributed to TC cell proliferation. It may be a promising target for gene therapy in human thyroid cancer.

Automated summary

The study revealed that elevated expression of eIF3a in human thyroid cancer is associated with tumor grade, and knockdown of eIF3a significantly reduces cell proliferation, increases apoptosis, and arrests cell cycle progression. These findings suggest that eIF3a may be a promising target for gene therapy in thyroid cancer.