title: Quinalizarin, a specific CK2 inhibitor, reduces cell viability and suppresses migration and accelerates apoptosis in different human lung cancer cell lines.
abstract: 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.
  
  
  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.
authors.forename: Y
authors.initials: Y
authors.lastname: Zhou
authors.forename: K
authors.initials: K
authors.lastname: Li
authors.forename: S
authors.initials: S
authors.lastname: Zhang
authors.forename: Q
authors.initials: Q
authors.lastname: Li
authors.forename: Z
authors.initials: Z
authors.lastname: Li
authors.forename: F
authors.initials: F
authors.lastname: Zhou
authors.forename: X
authors.initials: X
authors.lastname: Dong
authors.forename: L
authors.initials: L
authors.lastname: Liu
authors.forename: G
authors.initials: G
authors.lastname: Wu
authors.affiliation: Cancer Center, Huazhong University of Science and Technology, Wuhan 430023, China.
authors.forename: R
authors.initials: R
authors.lastname: Meng
mesh_terms: D000230:Adenocarcinoma / Q000188:drug therapy / Q000473:pathology; D017209:Apoptosis / Q000187:drug effects*; D018287:Carcinoma, Large Cell / Q000188:drug therapy / Q000473:pathology; D047390:Casein Kinase II / Q000037:antagonists & inhibitors*; D002465:Cell Movement / Q000187:drug effects*; D049109:Cell Proliferation / Q000187:drug effects*; D005434:Flow Cytometry; D006801:Humans; D008175:Lung Neoplasms / Q000188:drug therapy / Q000473:pathology*; D011799:Quinazolines / Q000494:pharmacology*; D055752:Small Cell Lung Carcinoma / Q000188:drug therapy / Q000473:pathology; D014407:Tumor Cells, Cultured
chemical_list: D011799:Quinazolines; D047390:Casein Kinase II