雷公藤红素通过PI3K/AKT信号通路抑制MMP3和MMP7，从而抑制结肠癌细胞的增殖和迁移。
Celastrol inhibits colorectal cancer cell proliferation and migration through suppression of MMP3 and MMP7 by the PI3K/AKT signaling pathway.
作者信息
Bufu Tang, Di Xu, Yilin Zhao, Gege Liang, Xi Chen, Ling Wang
机构信息
Department of Oncology, the First Affiliated Hospital of Dalian Medical University.
College of Medical Laboratory, Dalian Medical University, Dalian, People's Republic of China.
出版信息
Anticancer Drugs. 2018 Jul;29(6):530-538. doi: 10.1097/CAD.0000000000000621.
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.
结直肠癌（CRC）是最常见的恶性肿瘤之一。PI3K/AKT信号通路在CRC的发生和发展过程中，包括细胞增殖和迁移方面起着关键作用。雷公藤红素具有抗癌作用，但其机制尚待确定。在此，我们表明雷公藤红素可抑制CRC细胞的增殖和迁移。雷公藤红素处理还可降低PI3K/AKT信号通路相关成分以及MMP3和MMP7的表达水平。此外，敲低AKT而非mTOR可抑制MMP3和MMP7的表达水平，且AKT沉默可增强雷公藤红素对CRC细胞增殖和迁移的诱导作用。综上所述，这些发现表明雷公藤红素诱导的抗肿瘤作用是通过PI3K/AKT信号通路介导MMP3和MMP7实现的。
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