HCT116 인체 대장암 세포주에서 상백피 추출물에 의한 전이 억제 효과
Root Bark extract of Morus alba L. Suppressed the Migration and Invasion of HCT116 Human Colorectal Carcinoma Cells
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초록
The root bark of Morus alba L. (MA) used in traditional oriental medicine for the treatment of pulmonary diseases exerts various pharmacological activities including anticancer effects. In the current study, we investigated the effects of MA on the migration and invasion of colorectal carcinoma cells. Results from a transwell assay showed that the methylene chloride extract of MA (MEMA) suppressed the migration and invasion of HCT116 human colorectal carcinoma cells in a concentration-dependent manner. MEMA reduced both mRNA and protein levels of matrix metalloproteinase (MMP)-9, but did not suppress the expression of MMP-2 in HCT116 cells. As a molecular mechanism, MEMA inhibited the phosphorylation of mitogen-activated protein kinases (MAPKs), including ERK, JNK and p38, in a dose-dependent manner. In addition, MEMA dephosphorylated both Src and signal transducer and activator of transcription 3 (STAT3) in HCT116 cells. Taken together, we demonstrate that MEMA suppressed the migration and invasion capacity of HCT116 human colorectal cancer cells by downregulation of MMP-9 and inactivation of both MAPKs and Src/STAT3 signaling pathway.
Abstract
The root bark of Morus alba L. (MA) used in traditional oriental medicine for the treatment of pulmonary diseases exerts various pharmacological activities including anticancer effects. In the current study, we investigated the effects of MA on the migration and invasion of colorectal carcinoma cells. Results from a transwell assay showed that the methylene chloride extract of MA (MEMA) suppressed the migration and invasion of HCT116 human colorectal carcinoma cells in a concentration-dependent manner. MEMA reduced both mRNA and protein levels of matrix metalloproteinase (MMP)-9, but did not suppress the expression of MMP-2 in HCT116 cells. As a molecular mechanism, MEMA inhibited the phosphorylation of mitogen-activated protein kinases (MAPKs), including ERK, JNK and p38, in a dose-dependent manner. In addition, MEMA dephosphorylated both Src and signal transducer and activator of transcription 3 (STAT3) in HCT116 cells. Taken together, we demonstrate that MEMA suppressed the migration and invasion capacity of HCT116 human colorectal cancer cells by downregulation of MMP-9 and inactivation of both MAPKs and Src/STAT3 signaling pathway.
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