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Cellular Mechanisms of Targeting AKT of New Sulfonamide Tumor Inhibitor That Induces Apoptosis in BT549 Cells
Wang Guan1*, Chai Shaomeng2, Seria-Masole Shonyela3,Wang Mingyue3, Hao Mingyue3, Song Hongrui4, Shi Wei2
1Faculty of Agronomy, Jilin Agricultural University, Changchun 130118, China; 2College of Life Sciences, Jilin University, Changchun 130118, China; 3College of Animal Science and Technology, Jilin Agricultural University, Changchun 130118, China; 4Ministry of Education, Shenyang Pharmaceutical University, Shenyang 110016, China
Abstract: The abnormal PI3K/AKT signaling pathway accounts for tumorigenesis， metastasis and multidrug resistance， especially in breast cancer. In this article， we discovered a new sulfonamide tumor inhibitor， DHW-51， which induced the apoptosis in breast cancer cell line BT549. When p53 and PTEN were both knockdown in BT549， it showed that DHW-51 effectively inhibited the survival of BT549 cell in both dose-and time-dependent manner. The hemolytic test result indicated that DHW-51 had inconsiderable effect on normal cells when hemolytic activity of red blood cell showed less than 10% with 40 μmol/L of DHW-51. In addition， FACS results also suggested that DHW-51 induced apoptosis of BT549 cells significantly. They used flow cytometry to show that DHW-51 could significantly induce apoptosis of BT549 cells， the activity of caspase3 increased with 20 μmol/L of DHW-51， however， the expression of pro-caspase3 protein decreased. As showed in the results of Western blot， the phosphorylation level of AKT in BT549 cells decreased significantly， nevertheless， the expression level of the AKT protein was not affected. We speculated that DHW-51 induced apoptosis of BT540 by targeting AKT， and suggested DHW-51 was an AKT-targeted tumor inhibitor.
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