(2013) Suppression of OCT4B enhances sensitivity of lung adenocarcinoma A549 cells to cisplatin via increased apoptosis. Anticancer Research. pp. 5365-5374.
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Abstract
Background: Resistance to chemotherapy in lung adenocarcinoma remains a major obstacle. We examined the potential role of Octamer-binding transcription factor-4B (OCT4B) in enhancing sensitivity of lung adenocarcinoma cells to cisplatin. Materials and Methods: RNAi interference was used to examine the role of OCT4B in cisplatin-treated A549 cells. Cells were transfected with OCT4B siRNA prior to a 48-h cisplatin treatment. Propidium iodide (PI) and caspase-3 staining were used to determine cell viability and apoptosis. Cell-cycle analysis was performed to evaluate alterations in phase distribution. Results: OCT4B suppression in cells increased the number of non-viable, PI+, and apoptotic, caspase-3+ cells in the presence and absence of cisplatin treatment. Importantly, cisplatin treatment of OCT4B-suppressed cells resulted in a marked transition of cells from G0/G1 to G2/M phase. Conclusion: Silencing of OCT4B confers sensitivity to cisplatin treatment in A549 cells via cell-cycle regulation, increased proliferation and enhancement of cisplatin-induced apoptosis. OCT4B clearly protects A549 cells from apoptosis.
Item Type: | Article |
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Keywords: | caspase 3; cisplatin; octamer binding transcription factor 4B; octamer transcription factor 4; propidium iodide; RNA; unclassified drug, apoptosis; article; cancer cell; cancer chemotherapy; cell cycle G0 phase; cell cycle G1 phase; cell cycle G2 phase; cell cycle M phase; cell cycle S phase; cell viability; controlled study; drug sensitivity; human; human cell; immunoblotting; lung adenocarcinoma; priority journal; real time polymerase chain reaction; reverse transcription polymerase chain reaction; RNA extraction; RNA interference |
Page Range: | pp. 5365-5374 |
Journal or Publication Title: | Anticancer Research |
Volume: | 33 |
Number: | 12 |
Depositing User: | ms soheila Bazm |
URI: | http://eprints.ssu.ac.ir/id/eprint/8661 |
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