Research Papers:

Upregulation of CFTR in patients with endometriosis and its involvement in NFκB-uPAR dependent cell migration

Wenqing Huang, Aihong Jin, Jieting Zhang, Chaoqun Wang, Lai Ling Tsang, Zhiming Cai, Xiaping Zhou, Hao Chen and Hsiao Chang Chan _

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Oncotarget. 2017; 8:66951-66959. https://doi.org/10.18632/oncotarget.16441

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Wenqing Huang1,2,*, Aihong Jin4,*, Jieting Zhang1,2, Chaoqun Wang1,2, Lai Ling Tsang1,2, Zhiming Cai4, Xiaping Zhou4, Hao Chen1,2 and Hsiao Chang Chan1,2,3

1Epithelial Cell Biology Research Center, School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, PR China

2Institute of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, PR China

3Sichuan University – The Chinese University of Hong Kong Joint Laboratory for Reproductive Medicine, West China Second Hospital, Sichuan University, Chengdu, PR China

4Department of Gynecology, The Second People’s Hospital of Shenzhen, Shenzhen, PR China

*These authors have contributed equally to this work

Correspondence to:

Hsiao Chang Chan, email: [email protected]

Hao Chen, email: [email protected]

Keywords: endometriosis, CFTR, NFκB signaling, uPAR, cell migration

Received: January 17, 2017     Accepted: March 02, 2017     Published: March 22, 2017


Endometriotic tissues exhibit high migration ability with the underlying mechanisms remain elusive. Our previous studies have demonstrated that cystic fibrosis transmembrane conductance regulator (CFTR) acts as a tumor suppressor regulating cell migration. In the present study, we explored whether CFTR plays a role in the development of human endometriosis. We found that both mRNA and protein expression levels of CFTR and urokinase-type plasminogen activator receptor (uPAR) were significantly increased in ectopic endometrial tissues from patients with endometriosis compared to normal endometrial tissues from women without endometriosis and positively correlated. In human endometrial Ishikawa (ISK) cells, overexpression of CFTR stimulated cell migration with upregulated NFκB p65 and uPAR. Knockdown of CFTR inhibited cell migration. Furthermore, inhibition of NFκB with its inhibitors (curcumin or Bay) significantly reduced the expression of uPAR and cell migration in the CFTR-overexpressing ISK cells. Collectively, the present results suggest that the CFTR-NFκB-uPAR signaling may contribute to the progression of human endometriosis, and indicate potential targets for diagnosis and treatment.

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