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• W2537618892 abstract "// Yun-fang Zhen 1, * , Song-tao Li 2, * , Yun-rong Zhu 3, * , Xiao-dong Wang 1 , Xiao-zhong Zhou 2 , Lun-qing Zhu 1 1 The Center of Diagnosis and Treatment for Children’s Bone Diseases, The Children’s Hospital Affiliated to Soochow University, Suzhou, China 2 The Department of Orthopedics, The Second Affiliated Hospital of Soochow University, Suzhou, China 3 Department of Orthopedics, The Affiliated Jiangyin Hospital of Medical College of Southeast University, Jiangyin, China * These authors have contributed equally to this work Correspondence to: Lun-qing Zhu, email: zhulunqingszgk@163.com Xiao-dong Wang, email: xiaodongwangsz@163.com Xiao-zhong Zhou, email: zhouxiaozhongorth@163.com Keywords: osteosarcoma (OS), salinomycin, DNA-PKcs, microRNA-101, autophagy Received: September 09, 2016     Accepted: September 26, 2016     Published: October 17, 2016 ABSTRACT Malignant osteosarcoma (OS) is still a deadly disease for many affected patients. The search for the novel anti-OS agent is extremely urgent and important. Our previous study has proposed that salinomycin is a novel anti-OS agent. Here we characterized DNA-dependent protein kinase catalytic subunit (DNA-PKcs) as a primary salinomycin resistance factor in OS cells. DNA-PKcs inhibitors (NU7026, NU7441 and LY294002) or DNA-PKcs shRNA knockdown dramatically potentiated salinomycin-induced death and apoptosis of OS cells (U2OS and MG-63 lines). Further, forced-expression of microRNA-101 (“miR-101”) downregulated DNA-PKcs and augmented salinomycin’s cytotoxicity against OS cells. Reversely, over-expression of DNA-PKcs in OS cells inhibited salinomycin’s lethality. For the mechanism study, we show that DNA-PKcs is required for salinomycin-induced pro-survival autophagy activation. DNA-PKcs inhibition (by NU7441), shRNA knockdown or miR-101 expression inhibited salinomycin-induced Beclin-1 expression and autophagy induction. Meanwhile, knockdown of Beclin-1 by shRNA significantly sensitized salinomycin-induced OS cell lethality. In vivo , salinomycin administration suppressed U2OS xenograft tumor growth in severe combined immuno-deficient (SCID) mice, and its anti-tumor activity was dramatically potentiated with co-administration of the DNA-PKcs inhibitor NU7026. Together, these results suggest that DNA-PKcs could be a primary resistance factor of salinomycin in OS cells. DNA-PKcs inhibition or silence may thus significantly increase salinomycin’s sensitivity in OS cells." @default.
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• W2537618892 date "2016-10-17" @default.
• W2537618892 modified "2023-09-26" @default.
• W2537618892 title "Identification of DNA-PKcs as a primary resistance factor of salinomycin in osteosarcoma cells" @default.
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• W2537618892 doi "https://doi.org/10.18632/oncotarget.12712" @default.
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