@Article{096504016X14666990347554,
AUTHOR = {Sheng Li, Zhengli Cui, Xianfeng Meng},
TITLE = {Knockdown of PARP-1 Inhibits Proliferation and ERK Signals, Increasing Drug Sensitivity in Osteosarcoma U2OS Cells},
JOURNAL = {Oncology Research},
VOLUME = {24},
YEAR = {2016},
NUMBER = {4},
PAGES = {279--286},
URL = {http://www.techscience.com/or/v24n4/56976},
ISSN = {1555-3906},
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<sub>0</sub>/G<sub>1</sub> 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.},
DOI = {10.3727/096504016X14666990347554}
}