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Published on: October 9, 2015
Plasmid-encoding vasostatin inhibited the growth and metastasis of human hepatocellular carcinoma cells
Xing-Chen Peng1, Ming Wang, Xu-Xia Chen
1Department of Medical Oncology, Cancer Center, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, People's Republic of China, 443459664@qq.com.
Abstract:
The growth and metastasis of solid tumors depends on angiogenesis. Anti-angiogenesis therapy may represent a promising therapeutic option. Vasostatin, the N-terminal domain of calreticulin, is a very potent endogenous inhibitor of angiogenesis and tumor growth. In this study, we attempted to investigate whether plasmid-encoding vasostatin complexed with cationic liposome could suppress the growth and metastasis of hepatocellular carcinoma in vivo and discover its possible mechanism of action. Apoptosis induction of pSecTag2B-vasostatin plasmid on murine endothelial cells (MS1) was examined by flow cytometric analysis in vitro. Nude mice bearing HCCLM3 tumor received pSecTag2B-vasostatin, pSecTag2B-Null, and 0.9 % NaCl solution, respectively. Tumor net weight was measured and survival time was observed. Microvessel density within tumor tissues was determined by CD31 immunohistochemistry. H&E staining of lungs and TUNEL assay of primary tumor tissues were also conducted. The results displayed that pSecTag2B-vasostatin could inhibit the growth and metastasis of hepatocellular carcinoma xenografts and prolong survival time compared with the controls in vivo. Moreover, histologic analysis revealed that pSecTag2B-vasostatin treatment increased apoptosis and inhibited angiogenesis. The present data may be of importance to the further exploration of this new anti-angiogenesis approach in the treatment of hepatocellular cancer.
Insights
This study shows that plasmid-encoding vasostatin effectively suppresses hepatocellular carcinoma growth and metastasis in mice. This novel anti-angiogenesis therapy holds promise for treating liver cancer by inhibiting tumor development and prolonging survival.
Area of Science:
- Oncology
- Molecular Biology
- Gene Therapy
Background:
- Tumor growth and metastasis are dependent on angiogenesis.
- Anti-angiogenesis therapy is a promising strategy for cancer treatment.
- Vasostatin, derived from calreticulin, is a potent endogenous inhibitor of angiogenesis.
Purpose of the Study:
- To investigate the efficacy of plasmid-encoding vasostatin complexed with cationic liposome in suppressing hepatocellular carcinoma (HCC) growth and metastasis in vivo.
- To elucidate the mechanism of action of this novel anti-angiogenesis approach.
Main Methods:
- In vitro apoptosis induction assay using murine endothelial cells (MS1) treated with pSecTag2B-vasostatin.
- In vivo study in nude mice bearing HCCLM3 tumors, treated with pSecTag2B-vasostatin, pSecTag2B-Null, or saline.
- Assessment of tumor weight, survival time, microvessel density (CD31 staining), lung metastasis (H&E), and apoptosis (TUNEL assay).
Main Results:
- pSecTag2B-vasostatin significantly inhibited HCC xenograft growth and metastasis.
- Treatment with pSecTag2B-vasostatin prolonged survival time in tumor-bearing mice.
- Histologic analysis confirmed increased apoptosis and reduced angiogenesis in tumors treated with pSecTag2B-vasostatin.
Conclusions:
- Plasmid-encoding vasostatin complexed with cationic liposome demonstrates significant anti-tumor and anti-metastatic effects against hepatocellular carcinoma in vivo.
- The mechanism involves increased apoptosis and inhibition of angiogenesis.
- This approach represents a potential new anti-angiogenesis strategy for hepatocellular cancer treatment.
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