X Liu1, M Ma2, X Duan2, H Zhang2, M Yang2. 1. Key Laboratory of Cancer Prevention and Therapy, The Second Department of Thoracic Oncology, Tianjin Medical University Cancer Institute and Hospital, Tianjin's Clinical Research Center for Cancer, National Clinical Research Center for Cancer, Huanhuxi Road, Hexi District, Tianjin, 300060, China. drxmliu16@163.com. 2. Key Laboratory of Cancer Prevention and Therapy, The Second Department of Thoracic Oncology, Tianjin Medical University Cancer Institute and Hospital, Tianjin's Clinical Research Center for Cancer, National Clinical Research Center for Cancer, Huanhuxi Road, Hexi District, Tianjin, 300060, China.
Abstract
PURPOSE: Cisplatin is commonly used in non-small-cell lung cancer (NSCLC) chemotherapy; however, chemoresistance to cisplatin remains a great clinical challenge. Octamer-binding protein 4 (OCT4) has been reported to be overexpressed in NSCLC. In this study, we aimed to investigate the potential role of OCT4 in NSCLC with chemoresistance to cisplatin. METHODS: Expressions of OCT4 was detected in NSCLC tissues and cell lines. We utilized siRNA to knock down OCT4 expression in human NSCLC cells and analyzed their phenotypic changes. RESULTS: We found that the difference of OCT4 expression between NSCLC and the adjacent non-tumourous tissues was statistically significant. Knockdown of OCT4 in NSCLC cells could decrease cell proliferation, and potentiate apoptosis induced by cisplatin, suggesting OCT4 may contribute to cisplatin resistance in NSCLC. CONCLUSION: Our findings indicate that targeting OCT4 could improve cisplatin effect in NSCLC, confirming their role in modulating cisplatin sensitivity.
PURPOSE:Cisplatin is commonly used in non-small-cell lung cancer (NSCLC) chemotherapy; however, chemoresistance to cisplatin remains a great clinical challenge. Octamer-binding protein 4 (OCT4) has been reported to be overexpressed in NSCLC. In this study, we aimed to investigate the potential role of OCT4 in NSCLC with chemoresistance to cisplatin. METHODS: Expressions of OCT4 was detected in NSCLC tissues and cell lines. We utilized siRNA to knock down OCT4 expression in humanNSCLC cells and analyzed their phenotypic changes. RESULTS: We found that the difference of OCT4 expression between NSCLC and the adjacent non-tumourous tissues was statistically significant. Knockdown of OCT4 in NSCLC cells could decrease cell proliferation, and potentiate apoptosis induced by cisplatin, suggesting OCT4 may contribute to cisplatin resistance in NSCLC. CONCLUSION: Our findings indicate that targeting OCT4 could improve cisplatin effect in NSCLC, confirming their role in modulating cisplatin sensitivity.
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