Inhibiting effect of Endostar combined with ginsenoside Rg3 on breast cancer tumor growth in tumor-bearing mice

详细信息    查看全文

• 作者：Yun Zhang¹ ; Qing-Zhan Liu² ; Su-Ping Xing¹ ; ^{fenglin_w@126.com" class="auth_mail" title="E-mail the corresponding author} ; Jin-Ling Zhang¹
• 关键词：Breast cancer ; Recombinant human endostatin ; Ginsenoside Rg3 ; Autophagy
• 刊名：Asian Pacific Journal of Tropical Medicine
• 出版年：2016
• 出版时间：February 2016
• 年：2016
• 卷：9
• 期：2
• 页码：180-183
• 全文大小：267 K

文摘

To study the inhibiting effect of Endostar combined with ginsenoside Rg3 on breast cancer tumor growth in tumor-bearing mice.

Methods

Female mice were selected as experimental animals, and breast cancer tumor-bearing mouse models were established and then divided into groups A, B, C and D that respectively received saline, recombinant human endostatin, ginsenosides Rg3 and recombinant human endostatin combined with Rg3 intervention; 7 d, 14 d and 21 d after intervention, tumor tissue volume was measured; 21 d after intervention, mice were killed, tumor tissue was collected, and mRNA contents of angiogenesis molecules, invasion molecules, autophagy marker molecules and autophagy signaling pathway molecules were detected.

Results

At 7 d, 14 d and 21 d after intervention, tumor tissue volume of groups B, C and D was lower than that of group A, and tumor tissue volume of group D was lower than that of groups B and C; mRNA contents of VEGFA, VEGFB, VEGFC, MMP2, MMP9, p62, mTOR, PI3K, Akt, JNK and Beclin-1 in tumor tissue of groups B, C and D were significantly lower than those of group A, and LC3-II/LC3-I was significantly higher than that of group A; mRNA contents of VEGFA, VEGFB, VEGFC, MMP2, MMP9, p62, mTOR, PI3K, Akt, JNK and Beclin-1 in tumor tissue of group D were significantly lower than those of groups B and C, and LC3-II/LC3-I was higher than that of groups B and C.

Conclusions

Endostar combined with ginsenoside Rg3 has stronger inhibiting effect on breast cancer tumor growth in tumor-bearing mice than single drug, and it can inhibit angiogenesis and cell invasion, and enhance cell autophagy.