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Knockdown of PARP-1 Inhibits Proliferation and ERK Signals, Increasing Drug Sensitivity in Osteosarcoma U2OS Cells

Sheng Li, Zhengli Cui, Xianfeng Meng

Department of Orthopedics, Shengli Oilfield Central Hospital, Dongying, Shandong, China

Oncology Research 2016, 24(4), 279-286. https://doi.org/10.3727/096504016X14666990347554

Abstract

Poly(ADP-ribose) polymerase 1 (PARP-1) is reported to be involved in DNA repair and is now recognized as a key regulator in carcinogenesis. However, the potential role and the molecular mechanism underlying the effect of PARP-1 on osteosarcoma (OS) cells have not been elucidated. In this study, the results showed that knockdown of PARP-1 resulted in decreased cell proliferation, increased cell apoptosis, and G0/G1 phase arrest in U2OS cells. In addition, increased expression of active caspase 3 and Bax, but reduced Bcl-2, cyclin D1, and phosphorylated extracellular signal regulated kinase 1/2 (pERK1/2) were observed in PARP-1 knockdown in U2OS cells. Moreover, knockdown of PARP-1 correlated with elevated chemosensitivity of U2OS cells to cisplatin through inactivation of the ERK1/2 signaling pathway. In conclusion, our findings demonstrated that PARP-1 plays an important role in regulating OS growth, combining PARP-1 gene therapy with traditional chemotherapy, and may serve as a promising approach to OS therapy.

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APA Style
Li, S., Cui, Z., Meng, X. (2016). Knockdown of PARP-1 inhibits proliferation and ERK signals, increasing drug sensitivity in osteosarcoma U2OS cells. Oncology Research, 24(4), 279-286. https://doi.org/10.3727/096504016X14666990347554
Vancouver Style
Li S, Cui Z, Meng X. Knockdown of PARP-1 inhibits proliferation and ERK signals, increasing drug sensitivity in osteosarcoma U2OS cells. Oncol Res. 2016;24(4):279-286 https://doi.org/10.3727/096504016X14666990347554
IEEE Style
S. Li, Z. Cui, and X. Meng "Knockdown of PARP-1 Inhibits Proliferation and ERK Signals, Increasing Drug Sensitivity in Osteosarcoma U2OS Cells," Oncol. Res., vol. 24, no. 4, pp. 279-286. 2016. https://doi.org/10.3727/096504016X14666990347554



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