Abstract
BackgroundKIF18A is associated with a variety of tumours; however, the specific mechanism of action of KIF18A in hepatocellular carcinoma (HCC) remains unclear. In this study, in vitro and in vivo experiments were performed with the aim of exploring the potential function and molecular mechanism of kinesin KIF18A in the occurrence and development of HCC.MethodsWe detected the expression of KIF18A in tumour and adjacent tissues as well as cell proliferation, cell invasion and migration in hepatoma cells after silencing KIF18A. KIF18A-silenced hepatoma cells were subcutaneously injected into nude mice to verify the tumorigenicity of KIF18A. We also detected the expression of signal pathway-related proteins in hepatoma cells after KIF18A knockdown with the aim of exploring the association between KIF18A and related signalling pathways.ResultsThe level of KIF18A protein was higher in liver cancer tissues than adjacent tissues. After silencing KIF18A in SMMC-7721 and HepG2 cells, cell growth was obviously inhibited; the migration and invasion abilities were significantly decreased and the in vivo tumour weight was decreased compared to the control group (0.201 ± 0.088 g vs 0.476 ± 0.126 g, p = 0.009). The expression of cell cycle-related protein (cyclin B1), invasion and metastasis-related proteins (MMP-7 and MMP-9) and Akt-related proteins in hepatoma cells was also decreased after knocking down KIF18A.ConclusionsKIF18A may promote proliferation, invasion and metastasis of HCC cells by promoting the cell cycle signalling pathway as well as the Akt and MMP-7/MMP-9-related signalling pathways and may serve as a new target for the diagnosis and treatment of HCC.
Highlights
KIF18A is associated with a variety of tumours; the specific mechanism of action of KIF18A in hepatocellular carcinoma (HCC) remains unclear
Expression of KIF18A in tumour tissues and adjacent tissues Our previous experiments demonstrated the expression of KIF18A in human liver cancer tissue and paracancerous tissue at the mRNA level, and we show KIF18A protein expression in these tissues
After 48 h of culture, the scratch distances of HepG2 cells transfected with short hairpin RNA (shRNA)-KIF18A and shRNA-NC were 75 and 120 μm, respectively. These results showed that the migration ability of HCC cells transfected with shRNA-KIF18A was significantly lower than that of the shRNA-NC group after 24 and 48 h in culture
Summary
KIF18A is associated with a variety of tumours; the specific mechanism of action of KIF18A in hepatocellular carcinoma (HCC) remains unclear. In vitro and in vivo experiments were performed with the aim of exploring the potential function and molecular mechanism of kinesin KIF18A in the occurrence and development of HCC. The incidence and mortality of hepatocellular carcinoma (HCC) have been shown to be on the rise [1]. There has been some progress into understanding the aetiology, epidemiology, diagnosis, treatment and survival rate of HCC, but the prognosis of HCC is still poor and its pathogenesis remains unclear. We performed microarray analysis, PCR and immunohistochemical detection of HCC tissues and demonstrated that KIF18A is highly expressed in HCC [13].
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