Open Access
ARTICLE
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 G
0/G
1 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.
Keywords
Cite This Article
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