Cinobufacini Inhibits Colon Cancer Invasion and Metastasis via Suppressing Wnt/β-Catenin Signaling Pathway and EMT

转移 结直肠癌 MMP2型 Wnt信号通路 癌症研究 免疫印迹 MMP9公司 细胞周期蛋白D1 癌症 下调和上调 生物 信号转导 医学 内科学 细胞周期 基因 细胞生物学 生物化学
作者
Jie Wang,Han Cai,Qiaoli Liu,Yue Xia,Likai Xing,Qingsong Zuo,Yong Zhang,Cao Chen,Ke Xu,Peihao Yin,Teng Chen
出处
期刊:The American Journal of Chinese Medicine [World Scientific]
卷期号:48 (03): 703-718 被引量:107
标识
DOI:10.1142/s0192415x20500354
摘要

Cinobufacini is a well-known Chinese medicine extracted from Venenum Bufonis, also called Chan Su. It has been used clinically for various cancers, including colon cancer. However, the function of Cinobufacini on colon cancer invasion and metastasis, and its underlying molecular mechanism, is still not clear. In this study, we investigated the function and mechanism of Cinobufacini on colon cancer invasion and metastasis both in vitro and in vivo studies. Human colon cancer cells were cultured. CCK assay was used to detect the effect of Cinobufacini on colon cancer cells proliferation. The invasion and migration abilities were observed by transwell assays, and the expression of invasion and migration related genes MMP2, MMP9, and epithelial-to-mesenchymal transition (EMT) relate genes were observed by Western blot assays. An orthotopic xenograft model in nude mice was established using colon cancer HCT116 cells, and the function of Cinobufacini on colon cancer invasion and metastasis were observed in vivo. We found Cinobufacini significantly inhibited colon cancer cell proliferation in a dose/time-dependent manner; the invasion and migration abilities of colon cancer were decreased after treated with Cinobufacini. The metastasis and EMT related genes MMP9, MMP2, N-cadherin and Snail were obviously down-regulated, while the expression of E-cadherin was up-regulated after treatment with Cinobufacini. The Wnt/[Formula: see text]-catenin signaling pathway related genes were observed using WB,and results show that the expression of [Formula: see text]-catenin, wnt3a, c-myc, cyclin D1, and MMP7 were all down-regulated after being treated with cinobufacini, while the expression of APC was up-regulated. In vivo studies of the volume and weight of orthotopic xenograft tumors showed significantly shrinkage in the Cinobufacini group compared to the control group. The enterocoelia and liver metastasis tumors were significantly decreased, and the expression of MMP9, MMP2, and [Formula: see text]-catenin were also down-regulated, while E-cadherin was up-regulated in vivo after the treatment with Cinobufacini. Our data proves that Cinobufacini can inhibit colon cancer invasion and metastasis both in vitro and in vivo; the mechanism is related by suppressing the Wnt/[Formula: see text]-catenin signaling pathway and then inhibiting the EMT of CRC.
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