RON Mediates Tumor-Promoting Effects in Endometrial Adenocarcinoma.
RON Mediates Tumor-Promoting Effects in Endometrial Adenocarcinoma.
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RON 介导子宫内膜腺癌的促肿瘤作用
DOI:
10.1155/2021/2282916
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发表时间:
2021
影响因子:
--
通讯作者:
Zhang X
中科院分区:
文献类型:
--
作者:
Yu Q;Wang J;Li T;Xu X;Guo X;Ding S;Zhu L;Zou G;Chen Y;Zhang X
Endometrial adenocarcinoma is one of the most prevalent female reproductive tract cancers in the world, and the development of effective treatment is still the main goal of its current research. Epithelial-mesenchymal transition (EMT) plays a significant part in the occurrence and development of epithelial carcinoma, including endometrial adenocarcinoma. Recepteur d'origine nantais (RON) induces EMT and promotes proliferation, migration, and invasion in various epithelial-derived cancers, but its role in endometrial adenocarcinoma is still poorly studied. The purpose of this study is to verify the overexpression of RON in endometrial adenocarcinoma and to explore its specific roles. RON expression in tumor lesions was verified by immunohistochemical staining, HEC-1B cells were used to construct stable cell lines with RON overexpression or knockdown to investigate the effects of RON on the function of endometrial adenocarcinoma cells, and xenotransplantation experiment was carried out in nude mice to explore the effect of RON on the growth of endometrial adenocarcinoma in vivo. This study revealed that RON could promote the proliferation, migration, and invasion of HEC-1B cells and induce EMT, and these effects were regulated through the Smad pathway. RON overexpression could promote growth of endometrial adenocarcinoma cells in nude mice, while its inhibitor BMS777607 could restrict this role. RON played an important role in endometrial adenocarcinoma and had a potential to become a new therapeutic target for endometrial adenocarcinoma.
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影响因子:
9.7
作者:
Bourn JR;Ruiz-Torres SJ;Hunt BG;Benight NM;Waltz SE
通讯作者:
Waltz SE
DOI:
10.1016/j.ejogrb.2012.06.034
发表时间:
2012-11-01
影响因子:
2.6
作者:
Huang, Xiufeng;Chen, Liqing;Zhang, Xinmei
通讯作者:
Zhang, Xinmei
影响因子:
37.3
作者:
Ma Q;Guin S;Padhye SS;Zhou YQ;Zhang RW;Wang MH
通讯作者:
Wang MH
影响因子:
4.7
作者:
SAKURAGI, N;NISHIYA, M;FUJIMOTO, S
通讯作者:
FUJIMOTO, S
影响因子:
5.2
作者:
Kim, Sun-Ae;Lee, Kyung-Hwa;Yoon, Tae Mi
通讯作者:
Yoon, Tae Mi