RETRACTED: Knockdown of TMPRSS11D inhibits the proliferation, migration and invasion of cervical cancer cells (Retracted article. See vol. 11, pg. 5239, 2021)

被引:3
|
作者
Yan, Kun [2 ]
Hu, Chunyan [2 ]
Liu, Chen [2 ]
Chu, Guanghua [2 ]
Wang, Xinru [2 ]
Ma, Shuyun [3 ]
Li, Long [1 ]
机构
[1] Xi An Jiao Tong Univ, Affiliated Hosp 1, Dept Gynecol & Obstet, Xian 710061, Shaanxi, Peoples R China
[2] Northwest Women & Children Hosp, Dept Gynecol 2, Xian 710061, Shaanxi, Peoples R China
[3] Xian Med Univ, Affiliated Hosp 1, Dept Gynecol & Obstet, Xian 710077, Shaanxi, Peoples R China
关键词
TRYPSIN-LIKE PROTEASE; TRANSMEMBRANE SERINE PROTEASES; PI3K/AKT PATHWAY; PROGNOSIS; INSIGHTS; TARGET;
D O I
10.1039/c9ra02482d
中图分类号
O6 [化学];
学科分类号
0703 ;
摘要
TMPRSS11D is a member of the type II transmembrane serine proteases (TTSPs) family that is implicated in the development and progression of several cancers. However, the biological roles of TMPRSS11D in cervical cancer have not been investigated. In the present study, we detected the expression levels of TMPRSS11D in human cervical cancer tissues and cell lines. The results showed that TMPRSS11D expression was significantly upregulated in cervical cancer tissues as compared to the adjacent normal tissues. Besides, TMPRSS11D was highly expressed in human cervical cancer cell lines. Then we knocked down TMPRSS11D in cervical cancer cell lines to evaluate the effects of TMPRSS11D knockdown on cervical cancer cells. The results showed that knockdown of TMPRSS11D significantly suppressed cell proliferation, migration and invasion in cervical cancer cell lines. Furthermore, the data revealed that TMPRSS11D knockdown prevented epithelial-mesenchymal transition (EMT), as proved by the increased E-cadherin expression, as well as decreased N-cadherin and fibronectin expressions. Additionally, knockdown of TMPRSS11D inhibited the activation of the PI3K/Akt pathway in cervical cancer cells. Furthermore, insulin-like growth factor-1 (IGF-1) treatment reversed the inhibitory effects of TMPRSS11D knockdown on cell proliferation and migration. Collectively, knockdown of TMPRSS11D exerted anti-tumor activity, at least in part, via inhibiting the PI3K/Akt pathway. These findings indicated that TMPRSS11D might serve as a novel therapeutic target for the treatment of cervical cancer.
引用
收藏
页码:21591 / 21600
页数:10
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