@Article{096504018X15185747911701,
AUTHOR = {Fan-Chun Meng, Jun-Kai Lin},
TITLE = {Liquiritigenin Inhibits Colorectal Cancer Proliferation, Invasion,  and Epithelial-to-Mesenchymal Transition by Decreasing Expression  of Runt-Related Transcription Factor 2},
JOURNAL = {Oncology Research},
VOLUME = {27},
YEAR = {2019},
NUMBER = {2},
PAGES = {139--146},
URL = {http://www.techscience.com/or/v27n2/48638},
ISSN = {1555-3906},
ABSTRACT = {Inhibition of tumor metastasis is one of the most important purposes in colorectal cancer (CRC) treatment. This 
study aimed to explore the effects of liquiritigenin, a flavonoid extracted from the roots of Glycyrrhiza uralensis Fisch, on HCT116 cell proliferation, invasion, and epithelial-to-mesenchymal transition (EMT). We found 
that liquiritigenin significantly inhibited HCT116 cell proliferation, invasion, and the EMT process, but had no 
influence on cell apoptosis. Moreover, liquiritigenin remarkably reduced the expression of runt-related transcription factor 2 (Runx2) in HCT116 cells. Overexpression of Runx2 obviously reversed the liquiritigenininduced invasion and EMT inhibition. Furthermore, liquiritigenin inactivated the phosphoinositide 3-kinase/
protein kinase B (PI3K/AKT) pathway in HCT116 cells. Upregulation of Runx2 reversed the liquiritigenininduced PI3K/AKT pathway inactivation. In conclusion, our research verified that liquiritigenin exerted significant inhibitory effects on CRC invasion and EMT process by downregulating the expression of Runx2 and 
inactivating the PI3K/AKT signaling pathway. Liquiritigenin could be an effective therapeutic and preventative 
medicine for CRC treatment.},
DOI = {10.3727/096504018X15185747911701}
}