期刊
ONCOTARGET
卷 7, 期 2, 页码 1408-1420出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.6368
关键词
ovarian cancer; PDLIM2; DNA methylation; NOS2; nitric oxide signaling
资金
- National Natural Science Foundation of China [81402396]
- National Basic Research Program of China (973 program) [2013CB911300]
- Yi Yao Foundation [14H0563]
Ovarian cancer constitutes one of the most lethal gynaecological malignancies worldwide and currently no satisfactory therapeutic approaches have been established. Therefore, elucidation of molecular mechanisms to develop targeted therapy of ovarian cancer is crucial. PDLIM2 is critical to promote ubiquitination of nuclear p65 and thus its role in inflammation has been highlighted recently. We demonstrate that PDLIM2 is decreased in both ovarian high-grade serous carcinoma and in various human ovarian cancer cell lines compared with normal ovary tissues and human ovarian surface epithelial cells (HOSE). Further functional analysis revealed that PDLIM2 is epigenetically repressed in ovarian cancer development and inhibition of PDLIM2 promoted ovarian cancer growth both in vivo and in vitro via NOS2-derived nitric oxide signaling, leading to recruitment of M2 type macrophages. These results suggest that PDLIM2 might be involved in ovarian cancer pathogenesis, which could serve as a promising therapeutic target for ovarian cancer patients.
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