Hepatocellular carcinoma (HCC) is a common malignant tumor, and the risk factors of HCC is including chronic HBV and HCV infection, alcohol consumption, and aflatoxin. HCC have the character of strong invasion, as a result, it is a great threat to human health. Collectively, it is of great significance to explore the molecular mechanisms of the growth, invasion and metastasis of HCC, which can provide a theoretical basis for the molecular diagnosis, prognosis and treatment of HCC.
FBXO7 belongs to F-box protein family, which participates in the ubiquitin-proteasome system. In addition, FBXO7 is also involved in the regulation of cell cycle and is closely related to tumorigenesis and progression[22, 23], however, the role of FBXO7 in HCC is still elusive. In this study, the expression of FBXO7 in HCC cells was higher than that of normal liver cells, indicating that FBXO7 may play a role in the progression of HCC. In order to investigate the function of FBXO7 in HCC, FBXO7 was silenced by siRNA in this study. The results showed that silencing FBXO7 inhibited the cell proliferation, migration and invasion of hepatocellular carcinoma. Collectively, FBXO7 may play an oncogenic role in HCC development and progression. Moreover, the proportion of cells at G1 phase was increased and the proportion of cells at S phase was decreased after FBX07 was silenced, indicating that silencing FBXO7 in HCC cells might inhibit cell proliferation through promoting cell cycle arrest.
Autophagy is an intracellular degradation process in eukaryotes, among which ubiquitination plays an important role in the process of autophagy. As FBXO7 participates in the ubiquitin-proteasome system, we speculated that FBXO7 may play a part in the progression of HCC through autophagy. To verify this hypothesis, we detected the status of autophagy in HCC cells, the results showed that autophagy was enhanced after FBXO7 was silenced. However, autophagy has a bidirectional function in tumor cells, on the one hand, autophagy can prevent cell malignancy before the occurrence of tumor; on the other hand, autophagy can promote the growth of tumor after tumorigenesis. As a result, the role of autophagy induced by FBXO7 in HCC deserves further investigation.
In conclusion, FBXO7 may play an oncogenic role in hepatocellular carcinoma development and progression through autophagy. As a result, FBXO7 can be used as a biomarker for hepatocellular carcinoma, and further studies on the function and mechanism of FBXO7 will help to find new diagnostic and therapeutic methods of hepatocellular carcinoma. However, there are some limitations in this study that we only investigated the biological functions and mechanism of FBXO7 in vitro. The functional role of FBXO7 in vivo is required to explore in future.