Abstract
In the present study, the effect of Aurora-B inhibition on HepG2 cell invasion and migration in vitro was investigated. A recombinant plasmid targeting the Aurora-B gene (MiR-Aurora-B) was used to inhibit Aurora-B expression in HepG2 cells. Cell migration and invasion were investigated using Transwell migration and invasion assays. The results demonstrated that cell invasion and migration were suppressed by inhibiting Aurora-B. In addition, the effect of Aurora-B inhibition on the activity of the phosphoinositide 3-kinase (PI3K)/Akt/nuclear factor (NF)-κB signaling pathway was investigated by analyzing the protein expression levels of phosphorylated (p)-Akt, Akt, NF-κB p65, matrix metalloproteinase (MMP)-2 and MMP-9 using western blot analysis. The results demonstrated that the protein expression levels of p-Akt, NF-κB p65, MMP-2 and MMP-9 were reduced significantly by inhibiting Aurora-B. Therefore, inhibition of Aurora-B was shown to suppress hepatocellular carcinoma cell migration and invasion by decreasing the activity of the PI3K/Akt/NF-κB signaling pathway in vitro.
Highlights
Hepatocellular carcinoma (HCC) is the fifth most common malignancy worldwide [1,2]
The results revealed that the rates of invasion and migration in the cells transfected with MiR‐Aurora‐B were significantly lower compared with those transfected with MiR‐Neg (Fig. 2)
These results indicated that Aurora‐B inhibition was able to suppress HepG2 cell invasion and migration in vitro
Summary
Hepatocellular carcinoma (HCC) is the fifth most common malignancy worldwide [1,2]. surveillance of patients with risk factors for HCC and the development of locoregional treatment options have improved outcomes, to date, there are no effective curative methods due to the high invasion, Key words: Aurora-B, HepG2, invasion, migration, phosphoinositide 3‐kinase/Akt/nuclear factor-κB signaling pathway early metastasis and high tumor recurrence rates of HCC following surgery or interventional treatment. HCC progression, including metastasis, contributes to the high fatality rates of liver cancer. Lymph node metastasis of tumors is considered to be an important factor involved in HCC progression. The underlying molecular mechanisms involved in lymph node metastasis of HCC remain unclear. Aurora kinases are key regulators of protein phosphorylation during mitosis [3], consisting of three members that differ with regard to subcellular localization, activation kinetics and function. Accumulating evidence indicates that Aurora‐B is an important antitumor target that is strongly associated with lymph node metastasis in various tumor types [4,5,6,7]. The potential molecular mechanisms underlying the involvement of Aurora‐B in HCC development and lymph node metastasis remain unclear
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