BACKGROUND: Protein kinase CK2 is widely expressed in eukaryotic cells, and plays an important role in cell proliferation, migration, apoptosis, etc. The aim of the current study is to explore how Quinalizarin, a specific CK2 inhibitor, affects the cell proliferation, migration, and apoptosis of different pathological and genetic types of human lung cancer cell lines. MATERIALS AND METHODS: MTT assays were performed to evaluate the cell viability after being treated by Quinalizarin. Transwell migration assays were used to assess whether Quinalizarin could suppress cell migration. Flow cytometry was employed to test the apoptosis rate of different cells. RESULTS: After being treated by Quinalizarin, the viability of different pathological types of lung cancer cells (H446, H460, A549) were significantly suppressed in a time and dose-dependent manner. More interestingly, in a serial of human lung adenocarcinoma cell lines with different epidermal growth factor receptor (EGFR) mutation status, Quinalizarin was shown to have a much better ability to reduce the viability of cells with EGFR sensitive mutation than those with resistance mutations. Meanwhile, we also found that the cell migration of different pathological types of lung cancer cells (H446, H460, A549) was significantly decreased by Quinalizarin dose-dependently. In addition, the apoptosis rates in those cells were proved to be increased after exposed to Quinalizarin. CONCLUSIONS: Quinalizarin, the specific CK2 inhibitor, could reduce cell viability with emphasis on adenocarcinoma cells harboring EGFR sensitive mutation, suppresses migration, and accelerates apoptosis in different human lung cancer cell lines.
BACKGROUND: Protein kinase CK2 is widely expressed in eukaryotic cells, and plays an important role in cell proliferation, migration, apoptosis, etc. The aim of the current study is to explore how Quinalizarin, a specific CK2 inhibitor, affects the cell proliferation, migration, and apoptosis of different pathological and genetic types of humanlung cancer cell lines. MATERIALS AND METHODS:MTT assays were performed to evaluate the cell viability after being treated by Quinalizarin. Transwell migration assays were used to assess whether Quinalizarin could suppress cell migration. Flow cytometry was employed to test the apoptosis rate of different cells. RESULTS: After being treated by Quinalizarin, the viability of different pathological types of lung cancer cells (H446, H460, A549) were significantly suppressed in a time and dose-dependent manner. More interestingly, in a serial of humanlung adenocarcinoma cell lines with different epidermal growth factor receptor (EGFR) mutation status, Quinalizarin was shown to have a much better ability to reduce the viability of cells with EGFR sensitive mutation than those with resistance mutations. Meanwhile, we also found that the cell migration of different pathological types of lung cancer cells (H446, H460, A549) was significantly decreased by Quinalizarin dose-dependently. In addition, the apoptosis rates in those cells were proved to be increased after exposed to Quinalizarin. CONCLUSIONS:Quinalizarin, the specific CK2 inhibitor, could reduce cell viability with emphasis on adenocarcinoma cells harboring EGFR sensitive mutation, suppresses migration, and accelerates apoptosis in different humanlung cancer cell lines.