Isoliquiritigenin inhibits colorectal cancer cells HCT-116 growth by suppressing the PI3K/AKT pathway

Abstract

Isoliquiritigenin (ISL), a member of the flavonoids, is known to possess antitumor activity in different types of cancer including human breast cancer, hepatoma cancer, prostate cancer and others, both in vitro and in vivo. In the present study, we reported the effect of ISL on cell growth in human colorectal cancer cells HCT-116. As examined by CCK8 assays, ISL inhibited the proliferation of HCT-116 cells. Additionally, the antimigratory activity of ISL in HCT-116 cells was confirmed by trans-well chamber migration assays and invasion assays. Moreover, the results of fluorescence-activated cell sorting and Sodium Dodecyl Sulfate-Polyacrylamide Gel Electrophoresis (SDS-PAGE) analysis showed that ISL induced apoptosis in HCT-116 cells. Further detection using SDS-PAGE assay revealed that ISL decreased the levels of phospho-AKT (p-AKT), phospho-mTOR (p-mTOR), Cyclin D1 and phospho-p70S6 Kinase (p-P70S6K). Collectively, these findings indicated that isoliquiritigenin induced growth-inhibition and apoptosis through downregulating of PI3K/AKT in human colorectal cancer.