Coptisine suppresses tumor growth and progression by down-regulating MFG-E8 in colorectal cancer. Issue 54 (3rd September 2018)

• Record Type: Journal Article
• Authors: Cao, Qianyu; Hong, Shengwei; Li, Yuanyuan; Chen, Heng; Shen, Yining; Shao, Kang; Lu, Mengjie; Dai, Hui; Ma, Shitang; Dai, Guoliang
• Is Part Of: RSC advances. Volume 8:Issue 54(2018)
• Page Start: 30937
• Page End: 30945
• Publication Date: 2018-09-03
• Subjects: Chemistry -- Periodicals; 540.5
• DOI: 10.1039/c8ra05806g
• Languages: English
• ISSNs: 2046-2069

Abstract

Abstract : Treating colorectal cancer (CRC) continues to be a clinical challenge. Coptisine, an alkaloid derived from Coptis chinensis Franch. shows toxic effects on CRC cells, but its underlying mechanism remains elusive. Abstract : Treating colorectal cancer (CRC) continues to be a clinical challenge. Coptisine, an alkaloid derived from Coptis chinensis Franch. shows toxic effects on CRC cells, but its underlying mechanism remains elusive. MFG-E8 is involved in tumor growth and progression. Herein, we evaluated the effects of coptisine on MFG-E8 in CRC, and explored the mechanism. The expression of MFG-E8 in CRC and adjacent normal colon tissue samples from patients was detected. The effects of coptisine on CRC cells HCT116 in vitro were evaluated by CCK-8, adhesion and transwell assays. A xenograft tumor model was used to assess the effects of coptisine in vivo . The morphology of CRC tissue was observed by HE staining. Cell signaling was tested using western blotting and immunohistochemical assay. The expression of MFG-E8 in human CRC tissue samples significantly increased compared with that of adjacent normal ones. Coptisine significantly reduced the expressions of MFG-E8 in HCT116 cells and tumor-bearing mice. Moreover, coptisine suppressed the growth, adhesion and metastasis of CRC cells. Coptisine also suppressed the expression of MMP-2 and MMP-9 via the PI3K/AKT signaling pathway. Furthermore, it inhibited epithelial–mesenchymal transition in vivo and in vitro . Coptisine inhibited CRC growth and progression by down-regulating MFG-E8, and is a potential candidate for treatment.