Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

FOXQ1 promotes proliferation and metastasis of epithelial ovarian cancer via activation of SIRT1/NRF2 signaling pathway

Yinfeng Lv¹, Rongxia He¹ , Jia Liu¹, Aihong Wei¹, Ruijuan Chen²

¹The Obstetrics and Gynecology Department of Lanzhou University Second Hospital, Gansu; ²Lanzhou University, Gansu 730030, China.

For correspondence:- Rongxia He Email: herongxiapj6@126.com Tel:+869318942368

Accepted: 29 June 2019 Published: 28 July 2019

Citation: Lv Y, He R, Liu J, Wei A, Chen R. FOXQ1 promotes proliferation and metastasis of epithelial ovarian cancer via activation of SIRT1/NRF2 signaling pathway. Trop J Pharm Res 2019; 18(7):1397-1404 doi: 10.4314/tjpr.v18i7.5

© 2019 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the role of FOXQ1 in the progression of epithelial ovarian cancer and the underlying mechanism.

Methods: Forkhead Box Q1 overexpression was evaluated by quantitative reverse-transcription (qRT-PCR) in clinical epithelial ovarian cancer samples and cell lines. Proliferation, migration, and invasion of cancer cells were determined using CCK8, wound healing and transwell assay.

Results: FOXQ1 depletion inhibited the proliferation, migration, and invasion of `epithelial ovarian cancer cells. Moreover, FOXQ1 overexpression increased the amount of cells in S phase of the cell cycle, and FOXQ1 knockdown arrested cells inG1 phase. Results from ChIP and luciferase reporter assays showed that FOXQ1 was able to bind SIRT1 promoters. In addition, it was involved in sustaining the stability of nuclear factor erythroid derived 2-like 2 (NRF2) by decreasing its acetylation (p < 0.01), which was mediated by SIRT1. The data also demonstrated that NRF2 promotes proliferation, migration, and invasion of cancer cells upon FOXQ1 overexpression.

Conclusion: Forkhead Box Q1 contributes to the progression of epithelial ovarian cancer partly via SIRT1/NRF2 signaling pathway, this highlighting a novel strategy for treating epithelial ovarian cancer.

Keywords: Forkhead Box Q1, Nuclear factor erythroid 2-related factor 2, Epithelial ovarian cancer, Cell proliferation, Metastasis