The PARP inhibitor olaparib potentiates the effect of the DNA damaging agent doxorubicin in osteosarcoma

奥拉帕尼 PARP1 骨肉瘤 PARP抑制剂 阿霉素 癌症研究 聚ADP核糖聚合酶 DNA损伤 体内 医学 细胞凋亡 化疗 生物 DNA 内科学 聚合酶 生物化学 遗传学
作者
Hye Jeong Park,Jong Seok Bae,Kyoung Min Kim,Young Jae Moon,See‐Hyoung Park,Sung Ho Ha,Usama Khamis Hussein,Zhiqing Philippe Zhang,Ho Sung Park,Byung Hyun Park,Woo Sung Moon,Jung Ryul Kim,Kyu Yun Jang
出处
期刊:Journal of Experimental & Clinical Cancer Research [Springer Nature]
卷期号:37 (1) 被引量:69
标识
DOI:10.1186/s13046-018-0772-9
摘要

PARP1 facilitates the recovery of DNA-damaged cells by recruiting DNA damage response molecules such as γH2AX and BRCA1/2, and plays a role in resistance to antitumor therapies. Therefore, PARP inhibition being evaluated as an anti-cancer therapy. However, there are limited studies regrading PARP inhibition in osteosarcoma. We evaluated the expression of DNA damage response molecules in 35 human osteosarcomas and investigated the effects of co-treatment of the PARP inhibitor, olaparib, and doxorubicin in osteosarcoma cells. The expression patterns of PARP1, γH2AX, BRCA1, and BRCA2 were significantly associated with shorter survival of osteosarcoma patients. In osteosarcoma cells, knock-down of PARP1 and treatment of olaparib significantly inhibited proliferation of cells and induced apoptosis. Moreover, the anti-tumor effect was more significant with co-treatment of olaparib and doxorubicin in vitro and in vivo. This study suggests that combined use of a PARP inhibitor with doxorubicin, a DNA damaging agent, might be effective in the treatment of osteosarcoma patients, especially in the poor-prognostic subgroups of osteosarcoma expressing PARP1, γH2AX, or BRCA1/2.
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