Oncostatin M activates STAT3 to promote endometrial cancer invasion and angiogenesis
Oncostatin M activates STAT3 to promote endometrial cancer invasion and angiogenesis
复制标题
制瘤素 M 激活 STAT3 促进子宫内膜癌侵袭和血管生成。
DOI：
10.3892/or.2015.3951
复制
发表时间：
2015-07-01
期刊：
影响因子：
4.2
通讯作者：
Wan, Xiaoping
中科院分区：
文献类型：
--
作者：
Zhu, Minjiao;Che, Qi;Wan, Xiaoping
Oncostatin M (OSM), a pleiotropic cytokine, can either promote or inhibit the growth of tumors derived from specific tissues. However, little is known about the activity and expression pattern of OSM in endometrial cancers (ECs). Herein we show that expression of OSM in human ECs was significantly higher than that in hyperplastic or normal tissues. In EC tissues, high OSM levels were positively correlated with tumor stage, histological grade, myometrial invasion, and lymph node metastasis. Additionally, we demonstrated that recombinant human OSM (rhOSM) promoted tumor angiogenesis in EC cell lines by activating STAT3 (signal transducer and activator of transcription 3) and enhanced both cell migration and cell invasion. rhOSM did not, however, influence the proliferation of EC cells in vitro. In contrast, in our in vivo xenograft model, overexpression of rhOSM promoted cell proliferation, tumor growth, and angiogenesis in nude mice. Collectively, these experiments suggest that OSM may be a tumor promoter that encourages EC progression. OSM may thus serve as a potential target of antiangiogenic therapy for endometrial cancer.
