Research Article

Effect of recombinant human endostatin on the expression of c-Myc and bFGF in mouse gastric cancer cells

Published: May 18, 2015
Genet. Mol. Res. 14 (2) : 5258-5265 DOI: https://doi.org/10.4238/2015.May.18.17
Cite this Article:
Z.Y. Guo, G.D. Yao, L.P. Fu, Z.G. Fu, B. Hou (2015). Effect of recombinant human endostatin on the expression of c-Myc and bFGF in mouse gastric cancer cells. Genet. Mol. Res. 14(2): 5258-5265. https://doi.org/10.4238/2015.May.18.17
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Abstract

The aim of this study was to observe the effects of re­combinant human endostatin on the proliferation and apoptosis of mouse gastric cancer cells, and explore some possible mechanisms of recom­binant human endostatin inhibition of cancer. A murine gastric cancer xenograft model was established. A total of 20 mice were divided into two groups (control and experimental groups). The expression of c-Myc and basic fibroblast growth factor (bFGF) was determined by reverse transcription-polymerase chain reaction, Western blotting, and immu­nohistochemical staining methods. Tumor volume was measured and a growth curve was calculated. The tumor diameter in the experimental group was significantly smaller than that in the control group after treat­ment with endostatin for 21 days. The expression levels of c-Myc and bFGF in the experimental group were significantly lower than those of the control group (P < 0.05). There was a positive correlation between the expression of c-Myc and bFGF in the experimental group. Microvessel density was significantly inhibited in the experimental group (P < 0.05). These results demonstrated that recombinant human endostatin could in­hibit tumor metastasis by inhibition of the expression of c-Myc and bFGF in gastric cancer tissue as well as by inhibition of angiogenesis.

The aim of this study was to observe the effects of re­combinant human endostatin on the proliferation and apoptosis of mouse gastric cancer cells, and explore some possible mechanisms of recom­binant human endostatin inhibition of cancer. A murine gastric cancer xenograft model was established. A total of 20 mice were divided into two groups (control and experimental groups). The expression of c-Myc and basic fibroblast growth factor (bFGF) was determined by reverse transcription-polymerase chain reaction, Western blotting, and immu­nohistochemical staining methods. Tumor volume was measured and a growth curve was calculated. The tumor diameter in the experimental group was significantly smaller than that in the control group after treat­ment with endostatin for 21 days. The expression levels of c-Myc and bFGF in the experimental group were significantly lower than those of the control group (P

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