P-0008 - Effect on the proliferation, invasion and metastasis of gastric cancer cells transfected by metastasis suppressor gene kiss-1 in vivo

Date 28 June 2014
Event World GI 2014
Session Poster Session
Topics Basic Science
Gastric Cancer
Translational Research
Presenter XiaoBin Hu
Citation Annals of Oncology (2014) 25 (suppl_2): ii14-ii104. 10.1093/annonc/mdu165
Authors X. Hu
  • Department of Gastrointestinal Tumor Pathology of Cancer Institute and General Surgery Institute, The First Hospital of China Medical University, Shenyang/CN

Abstract

Introduction

Recent studies have found kiss-1 gene to be a new tumor metastasis suppressor gene, associated with a variety of tumor invasion and metastasis. Our previous study found that kiss-1 gene can suppress the proliferation, colony formation, migration and invasion of gastric cancer cells in vitro. This study aimed to further explore the effects of kiss-1 gene on gastric cancer growth and organic metastasis in vivo, as well as investigate related mechanisms.

Methods

In this study, the growth of subcutaneous xenografts and lung, liver metastasis of hematogenous disseminated gastric cancer cell in nude mice was used to evaluate the effect on the growth and metastasis of gastric cancer cells transfected by kiss-1 gene in vivo. We detected the levels of Ki67, Sp1 and VEGF protein by immunohistochemical staining and evaluated microvessel density (MVD) by CD31 marker on subcutaneous xenografts. Liver and lung metastases count were used to evaluate the effect on organic metastasis of kiss-1 gene.

Results

Kiss-1 gene significantly suppressed the growth of gastric xenografts and lung, liver metastasis of hematogenous disseminated gastric cancer cell in nude mice, reduced Sp1, VEGF protein expression and xenografts microvessel density in vivo.

Conclusion

Kiss-1 gene significantly suppressed the growth and metastasis of gastric cancer cell in nude mice, mechanisms of which were involved with that kiss-1 gene down-regulated transcription factor Sp1 and inhibited VEGF transcription, thereby suppressed tumor angiogenesis.