Effects of Trigger Transposable Element-Derived 1 on the Growth of Hepatocellular Carcinoma

Cell cycle dysregulation is one of the most important hallmarks of cancer. Bioinformatics studies have suggested that trigger transposable element-derived 1 (TIGD1) is expressed at higher levels in the tumor tissues from the clinical hepatocellular carcinoma (HCC) samples and may be related to the cell cycle. However, the underlying mechanism is unclear. To explore the specific mechanism of TIGD1 regulating the growth of hepatocellular carcinoma cells, this paper first analyzed the growth of HCC cell line Hep3B with TIGD1 knockdown by using shRNA plasmid. The results show that cell growth is inhibited. Then, cell cycle analysis by flow cytometry was used to investigate the effect of TIGD1 knockdown on cell cycle of HCC. The results show that the cell cycle progression of the Hep3B cell line is mainly blocked in the G2/M phase. Next, Immunoprecipitation (IP) experiments were used to verify the protein molecules with which TIGD1 might interact. And the results show that TIGD1 may be bound to Aurora kinase interacting protein 1 (AURKAIP1). Further, the Co-IP experiment confirmed the interaction between TIGD1 and AURKAIP1. AURKAIP1 is known to regulate the proteasomal degradation pathway of Aurora kinase A (AURKA), and AURKA is a mitotic regulatory protein that is closely associated with cell cycle progression. The paper further explored the effect of TIGD1 on AURKA protein levels, and the results show that TIGD1 knockdown obviously decreases the protein level of AURKA without affecting its mRNA level in Hep3B cells. In conclusion, TIGD 1 may affect cell cycle progression by regulating the post-transcriptional levels of AURKA in HCC cells, thus affecting the development of HCC.