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Impact of Butein on Apoptosis, Migration, Invasion, and Epithelial-Mesenchymal Transitions of HT-29 Human Colon Cancer Cells

Author(s): Q. Yang, X. Shi, Xiaoying Wang, Donglin Zhao, J. Fan, Tian Li, C. Fan and S. Ning*
Department of Pharmacy, Graduate School of Hebei North University, Qiaodong, Zhangjiakou 075000, 1Department of Gastroenterology, Air Force Medical Center, Haidian Beijing 100142, China

Correspondence Address:
S. Ning, Department of Gastroenterology, Air Force Medical Center, Haidian Beijing 100142, China, E-mail:

The aim of this research is to investigate the impact of butein on apoptosis, migration, invasion, and epithelial-mesenchymal transition in HT-29 colon cancer cells. HT-29 cancer cells were introduced into the suitable cell culture plates according to their density, and we exposed the cells to varying dose of butein for 24 h. Through the utilization of cell counting kit-8 assays, cell scratch, and cell invasion assays, we assessed the cells’ functionality, movement, and invasion capacity. The levels of apoptosis-related proteins B-cell lymphoma 2 and B-cell lymphoma 2 associated X, epithelial-mesenchymal transition-related proteins E-cadherin, N-cadherin, and snail, along with the growth arrest-specific 6 protein, were identified using Western blot. The proliferation, migration, and invasion of HT-29 cells were significantly suppressed by butein, along with the reduction in B-cell lymphoma 2 expression and B-cell lymphoma 2/B-cell lymphoma 2 associated X ratios (p<0.05). Furthermore, butein suppressed the expression of N-cadherin, enhanced the expression of E-cadherin, and inhibited the expression of snail, which is their upstream regulator (p<0.05). Additionally, we discovered that butein suppressed the expression of growth arrest-specific 6 (p<0.05). In conclusion, butein inhibited the proliferation, migration, invasion and promoted apoptosis, which may be related to the reversal of epithelial-mesenchymal transition process of HT-29 cells and this process, may be related to the inhibition the expression of growth arrest-specific 6 by butein.

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