Celastrol inhibits colorectal cancer cell proliferation and migration through suppression of MMP3 and MMP7 by the PI3K/AKT signaling pathway

被引:62
作者
Tang Bufu [1 ]
Xu Di [1 ]
Zhao Yilin [2 ]
Liang Gege [1 ]
Chen Xi [1 ]
Wang Ling [1 ]
机构
[1] Dalian Med Univ, Affiliated Hosp 1, Dept Oncol, Dalian, Peoples R China
[2] Dalian Med Univ, Coll Med Lab, Dalian, Peoples R China
关键词
AKT; celastrol; colorectal cancer; MMP3; MMP7; TUMOR-GROWTH; HEPATOCELLULAR-CARCINOMA; INDUCED APOPTOSIS; DOWN-REGULATION; INVASION; TRITERPENE; EXPRESSION; SURVIVAL; COLON;
D O I
10.1097/CAD.0000000000000621
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Colorectal cancer (CRC) is one of the most frequent malignant tumors. Signaling by the PI3K/AKT pathway is crucial for CRC development and progression, including proliferation and migration. Celastrol has an anticancer effect, but its mechanism needs to be determined. Here, we showed that celastrol suppressed CRC cell proliferation and migration. Celastrol treatment also decreased the PI3K/AKT pathway components, and MMP3 and MMP7 expression levels. In addition, knockdown of AKT, not mTOR, inhibited MMP3 and MMP7 expression levels and AKT silencing promoted the celastrol-induced effects on CRC cell proliferation and migration. Taken together, these findings indicated that the celastrol-induced antitumor effects were mediated through MMP3 and MMP7 by the PI3K/AKT signaling pathway.
引用
收藏
页码:530 / 538
页数:9
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