Abstract
BackgroundTo understand the involvement of structural maintenance of chromosome 4 (SMC4) in the development and progression of hepatocellular carcinoma (HCC).MethodsReal-time quantitative PCR and Western Blotting were applied to measure the expression of SMC4 in HCC samples and cell lines. The tumor-promoting effect of SMC4 was determined by WST-1, soft agar colony formation, cell motility and invasion assays. The SMC4 target signal pathway was identified by luciferase reporter and real-time quantitative PCR assays.ResultsThe upregulation of SMC4 was frequently detected in HCC samples and cell lines. Functional assays demonstrated that SMC4 could effectively promote tumor cell growth rate, colony formation in soft agar, wound-healing and invasion. Further studies showed that increased miR-219 levels caused a significant decrease in the SMC4 expression, and SMC4 inhibitor downregulated JAK2/Stat3 expression at both the mRNA and protein levels.ConclusionsOur findings provide new insight into SMC4 function and the mechanisms of growth and invasion of HCC.
Highlights
Hepatocellular carcinoma (HCC) is the most common primary liver cancer, and the third most deadly type of cancer globally, following lung and stomach cancers [1]
structural maintenance of chromosome 4 (SMC4) is strongly upregulated in hepatocellular carcinoma (HCC) Real-time quantitative PCR and Western Blotting were performed to determine the expression of SMC4 in 4 HCC cell lines (97-H, HepG2, Bel-7405, and smmc7721) and 4 primary HCC samples
The results showed that SMC4 was strongly upregulated in 4 HCC cell lines compared to normal cells (L02), and highly expressed in 4 primary HCC samples compared to paracancerous and non-tumor samples (Figure 1)
Summary
Hepatocellular carcinoma (HCC) is the most common primary liver cancer, and the third most deadly type of cancer globally, following lung and stomach cancers [1]. Small HCCs are amenable to more effective treatment [5,6]. HCC is diagnosed at advanced stages in most patients when only limited therapeutic options are available. HCC is a highly heterogeneous tumor [7]. Recent studies have demonstrated the importance of the JAK/STAT pathway in the development of HCC, and suggest that the use of JAK/STAT inhibitors might have potential in the treatment of HCC [16]. Identification of the predominant molecular mechanisms as therapeutic options for HCC is a research area of great importance and interest. To understand the involvement of structural maintenance of chromosome 4 (SMC4) in the development and progression of hepatocellular carcinoma (HCC)
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