AKT/mTOR Down-regulation by CX-4945, a CK2 Inhibitor, Promotes Apoptosis in Chemorefractory Non-small Cell Lung Cancer Cells
- Authors
- So, Kwang Sup; Rho, Jin Kyung; Choi, Yun Jung; Kim, Seon Ye; Choi, Chang Min; Chun, Young Jin; Lee, Jae Cheol
- Issue Date
- Mar-2015
- Publisher
- INT INST ANTICANCER RESEARCH
- Keywords
- CK2; AKT/mTOR; chemorefractory; lung cancer
- Citation
- ANTICANCER RESEARCH, v.35, no.3, pp 1537 - 1542
- Pages
- 6
- Journal Title
- ANTICANCER RESEARCH
- Volume
- 35
- Number
- 3
- Start Page
- 1537
- End Page
- 1542
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/9835
- ISSN
- 0250-7005
1791-7530
- Abstract
- Aim: The response to chemotherapeutic drugs in non-small cell lung cancer (NSCLC) is unsatisfactory, leading to poor outcomes. This study the aimed to investigates anticancer effects of CX-4945, a potent casein kinase II (CK2) inhibitor, in chemorefractory NSCLC cells. Materials and Methods: Cell proliferation and apoptosis assay were carried-out by annexin V-FITC and FACScan after drug treatment with paclitaxel, cisplatin and CX-4945. AKT/mTOR and CK2 alpha signals were measured by western blotting. Treatment was carried-out using siRNA to inhibit CK2 alpha. Results: Paclitaxel. and cisplatin effectively inhibited cell proliferation and induced apoptosis in A549 cells, while not in H1299, Calu-1 and H358 cells. In these chemorefractory cell lines, AKT signalling was maintained despite drug treatment. However, CX-4945 suppressed cell growth, with cell-cycle arrest at G(2)/M phase and induced apoptosis with an increase of cleaved caspase-3 and PARP1 in a dose-dependent manner. Accordingly. AKT and its downstream signals such as mTOR and p70S6K were down-regulated by CX-4945. Transfection of CK2 alpha siRNA had similar effects to CX-4945 treatment on cell proliferation and apoptosis. Conclusion: CX-4945 shows a promising anticancer action through down-regulation of AKT/mTOR signals. suggesting its possible application for treatment of chemorefractory lung cancer.
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