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Abstract
Aim Microvessel density is a marker of tumor angiogenesis activity for development and metastasis. Our preliminary study showed that ginsenoside Rg3 (Rg3) induces apoptosis in hepatocellular carcinoma (HCC) in vitro. The aim of this study was to investigate the cross-link for apoptosis induction and antiangiogenesis effect of Rg3 on orthotopic HCC in vivo. Methods The murine HCC cells Hep1-6 were implanted in the liver of mouse. With oral feeding of Rg3 (10 mg/kg once a day for 30 days), the quantitative analysis of apoptosis was performed by using pathology and a transmission electron microscope and microvessel density was quantitatively measured by immunohistochemical staining of the CD105 antibody. The mice treated with Rg3 (n = 10) were compared with the control (n = 10) using Kaplan-Meier analysis. Animal weight and tumor weight were measured to determine the toxicity of Rg3 and antitumor effect on an orthotopic HCC tumor model. Results With oral feeding of Rg3 daily in the first 30 days on tumor implantation, Rg3 significantly decreased the orthotopic tumor growth and increased the survival of animals (P < 0.05). Rg3-treated mice showed a longer survival than the control (P < 0.05). Rg3 treatment induced apoptosis and inhibited angiogenesis. They contributed to the tumor shrinkage. Rg3 initialized the tumor apoptotic progress, which then weakened the tumor volume and its capability to produce the vascularized network for further growth of the tumor and remote metastasis. Conclusion Rg3 inhibited the activation of microtumor vessel formation in vivo besides its apoptosis induction. Rg3 may be used as an adjuvant agent in the clinical HCC treatment regimen.
Highlights
Hepatocellular carcinoma (HCC) is one of the fifth most common cancers worldwide and the third most common cause of cancer death [1,2,3]
Because HCC is generally originated from chronic hepatitis and many patients suffer from cirrhosis, the treatment is even more challenging than other malignancies
The programmed cell death controlled by caspase protease activation was found in the in vitro HCC cells and other tumors
Summary
Hepatocellular carcinoma (HCC) is one of the fifth most common cancers worldwide and the third most common cause of cancer death [1,2,3]. HCC is a highly vascularized tumor, and the antiangiogenesis treatments such as arterializations and embolization have been applied; the overall clinical effect is not satisfying [4]. The metastasis and recurrence of hepatocellular carcinoma are still very challenging [5, 6]. HCC is especially highly prevalent in China, mainly attributed to the prevalence of hepatitis B virus (HBV) persistent infection and HBV-induced cirrhosis [7, 8]. Because HCC is generally originated from chronic hepatitis and many patients suffer from cirrhosis, the treatment is even more challenging than other malignancies. The effect and the toxicity are two sides that must be conjointly balanced
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