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Protein tyrosine phosphatase L1 inhibits high-grade serous ovarian carcinoma progression by targeting IκBα

Authors Wang Y, Li M, Huang T, Li J

Received 2 March 2018

Accepted for publication 26 May 2018

Published 30 October 2018 Volume 2018:11 Pages 7603—7612


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 3

Editor who approved publication: Dr Samir Farghaly

Yacheng Wang, Miao Li, Ting Huang, Jun Li

Department of Oncology, The Central Hospital of Wuhan, Wuhan, Hubei, China

Background: High-grade serous ovarian cancer (HGSOC) represents most of the ovarian cancers and accounts for 70%–80 % of related deaths. The overall survival of HGSOC has not been remarkably improved in the past decades, due to the tumor dissemination in peritoneal cavity and invasion of adjacent organs. Therefore, identifying molecular biomarkers is invaluable in helping predicting clinical outcomes and developing targeted chemotherapies. Although there have been studies revealing the prognostic significance of protein tyrosine phosphatase L1 (PTPL1) in breast cancer and lung cancer, its involvement and functions in HGSOC remains to be elucidated.
Methods: We retrospectively enrolled a cohort of HGSOC patients after surgical resection. And analyzed the mRNA and protein levels of PTPL1 in tissue samples.
Results: We found that PTPL1 presented a lower expression in HGSOC tissues than in adjacent normal ovarian tissues. Besides, the PTPL1 level was negatively correlated with tumor stage, implying its potential role as a tumor suppressor. Univariate and multivariate analyses identified that patients with higher PTPL1 showed a better overall survival compared to those with lower PTPL1 expression. In addition, cellular experiments confirmed the role of PTPL1 in suppressing tumor proliferation and invasion. Furthermore, we demonstrated that PTPL1 negatively regulated phosphorylation of tyrosine 42 on IκBα (IκBα-pY42). To our knowledge, this is the initial finding on PTPL1 targeting IκBα-pY42 site. Finally, our data indicated that PTPL1 suppressed tumor progression by dephosphorylating IκBα-pY42, which stabilized IκBα and attenuated nucleus translocation of NF-κB.
Conclusion: Our study revealed a tumor-suppressing role of PTPL1 in HGSOC by targeting IκBα.

Keywords: IκBα, phosphorylation, prognosis, PTPL1, serous ovarian carcinoma, overall survival

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