Abstract

Selenoprotein P (SEPP1) is a kind of secretory glycoproteins with an antioxidant effect during the development of some diseases. In this study, we attempted to observe the expression of SEPP1 in livers from the patients with hepatocellular carcinoma (HCC) and explore its effect on HCC cells. All the tissues from patients with HCC were obtained from Affiliated Hospital of Nantong University. Western blot and immunohistochemical results showed that SEPP1 was reduced in HCC liver tissues. Its expression was negatively correlated with Ki67 expression in tissues. The expression of SEPP1 in normal liver cell line was significantly higher than those in the liver cancer cell lines. Serum starvation and release experiment demonstrated that SEPP1 expression was reduced and PCNA expression was increased, when the serum was re-added into cell culture system and the cells were on a proliferation state. After SEPP1 over-expression plasmid was transfected into HepG2 cells, cell proliferation of HepG2 cells and PCNA expression level were all inhibited by SEPP1. Results obtained via 8-isoprostane ELISA further indicated that inhibited ROS level was found in HepG2 cells transfected with SEPP1 over-expression plasmid. In addition, RT-qPCR results demonstrated that GPX1 expression levels increased in HepG2 cells transfected with SEPP1 over-expression plasmid. In conclusion, SEPP1 may inhibit the proliferation of HCC cells, accompanied by the reduction of ROS production and the increasing of GPX1 expression.

Highlights

  • Hepatocellular carcinoma (HCC) is one of the most common cancers which could induce death worldwide

  • We found that the expression of Selenoprotein P (SEPP1) protein was down-regulated in HCC tissues, compared to that in the adjacent tissues and in the normal tissues (Fig 1A)

  • Both the results obtained from Li et al and us were all demonstrated that the expression of SEPP1 was low in HCC patients

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Summary

Introduction

Hepatocellular carcinoma (HCC) is one of the most common cancers which could induce death worldwide. Hepatitis B virus (HBV) infection could induce the accumulation of mitochondrial reactive oxygen species (ROS), thereby inhibiting the expression of suppressor of cytokine signaling 3 (SOCS3) and activating the interleukin-6 (IL-6)/STAT3 pathway,

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