Maelstrom promotes tumor metastasis through regulation of FGFR4 and epithelial-mesenchymal transition in epithelial ovarian cancer

Abstract Background Increasing evidence has indicated that Maelstrom (MAEL) plays an oncogenic role in various human carcinomas. However, the exact function and mechanisms by which MAEL acts in epithelial ovarian cancer (EOC) remain unclear. Results This study demonstrated that MAEL was frequently o...

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Main Authors: Wei-Peng He, Gui-Ping Yang, Zun-Xian Yang, Hong-Wei Shen, Ze-Shan You, Guo-Fen Yang
Format: Article
Language:English
Published: BMC 2022-05-01
Series:Journal of Ovarian Research
Subjects:
Online Access:https://doi.org/10.1186/s13048-022-00992-4
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author Wei-Peng He
Gui-Ping Yang
Zun-Xian Yang
Hong-Wei Shen
Ze-Shan You
Guo-Fen Yang
author_facet Wei-Peng He
Gui-Ping Yang
Zun-Xian Yang
Hong-Wei Shen
Ze-Shan You
Guo-Fen Yang
author_sort Wei-Peng He
collection DOAJ
description Abstract Background Increasing evidence has indicated that Maelstrom (MAEL) plays an oncogenic role in various human carcinomas. However, the exact function and mechanisms by which MAEL acts in epithelial ovarian cancer (EOC) remain unclear. Results This study demonstrated that MAEL was frequently overexpressed in EOC tissues and cell lines. Overexpression of MAEL was positively correlated with the histological grade of tumors, FIGO stage, and pT/pN/pM status (p < 0.05), and it also acted as an independent predictor of poor patient survival (p < 0.001). Ectopic overexpression of MAEL substantially promoted invasiveness/metastasis and induced epithelial-mesenchymal transition (EMT), whereas silencing MAEL by short hairpin RNA effectively inhibited its oncogenic function and attenuated EMT. Further study demonstrated that fibroblast growth factor receptor 4 (FGFR4) was a critical downstream target of MAEL in EOC, and the expression levels of FGFR4 were significantly associated with MAEL. (P < 0.05). Conclusion Our findings suggest that overexpression of MAEL plays a crucial oncogenic role in the development and progression of EOC through the upregulation of FGFR4 and subsequent induction of EMT, and also provide new insights on its potential as a therapeutic target for EOC.
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spelling doaj.art-44d369d12f81412298b2ca12d46355ff2023-01-03T07:25:43ZengBMCJournal of Ovarian Research1757-22152022-05-0115111010.1186/s13048-022-00992-4Maelstrom promotes tumor metastasis through regulation of FGFR4 and epithelial-mesenchymal transition in epithelial ovarian cancerWei-Peng He0Gui-Ping Yang1Zun-Xian Yang2Hong-Wei Shen3Ze-Shan You4Guo-Fen Yang5Department of Gynecology, the First Affiliated Hospital, Sun Yat-Sen UniversityDepartment of Gynecology, the First Affiliated Hospital, Sun Yat-Sen UniversityDepartment of Gynecology, the First Affiliated Hospital, Sun Yat-Sen UniversityDepartment of Gynecology, the First Affiliated Hospital, Sun Yat-Sen UniversityDepartment of Gynecology, the First Affiliated Hospital, Sun Yat-Sen UniversityDepartment of Gynecology, the First Affiliated Hospital, Sun Yat-Sen UniversityAbstract Background Increasing evidence has indicated that Maelstrom (MAEL) plays an oncogenic role in various human carcinomas. However, the exact function and mechanisms by which MAEL acts in epithelial ovarian cancer (EOC) remain unclear. Results This study demonstrated that MAEL was frequently overexpressed in EOC tissues and cell lines. Overexpression of MAEL was positively correlated with the histological grade of tumors, FIGO stage, and pT/pN/pM status (p < 0.05), and it also acted as an independent predictor of poor patient survival (p < 0.001). Ectopic overexpression of MAEL substantially promoted invasiveness/metastasis and induced epithelial-mesenchymal transition (EMT), whereas silencing MAEL by short hairpin RNA effectively inhibited its oncogenic function and attenuated EMT. Further study demonstrated that fibroblast growth factor receptor 4 (FGFR4) was a critical downstream target of MAEL in EOC, and the expression levels of FGFR4 were significantly associated with MAEL. (P < 0.05). Conclusion Our findings suggest that overexpression of MAEL plays a crucial oncogenic role in the development and progression of EOC through the upregulation of FGFR4 and subsequent induction of EMT, and also provide new insights on its potential as a therapeutic target for EOC.https://doi.org/10.1186/s13048-022-00992-4Ovarian cancerMaelstromEMTMetastasisFGFR4
spellingShingle Wei-Peng He
Gui-Ping Yang
Zun-Xian Yang
Hong-Wei Shen
Ze-Shan You
Guo-Fen Yang
Maelstrom promotes tumor metastasis through regulation of FGFR4 and epithelial-mesenchymal transition in epithelial ovarian cancer
Journal of Ovarian Research
Ovarian cancer
Maelstrom
EMT
Metastasis
FGFR4
title Maelstrom promotes tumor metastasis through regulation of FGFR4 and epithelial-mesenchymal transition in epithelial ovarian cancer
title_full Maelstrom promotes tumor metastasis through regulation of FGFR4 and epithelial-mesenchymal transition in epithelial ovarian cancer
title_fullStr Maelstrom promotes tumor metastasis through regulation of FGFR4 and epithelial-mesenchymal transition in epithelial ovarian cancer
title_full_unstemmed Maelstrom promotes tumor metastasis through regulation of FGFR4 and epithelial-mesenchymal transition in epithelial ovarian cancer
title_short Maelstrom promotes tumor metastasis through regulation of FGFR4 and epithelial-mesenchymal transition in epithelial ovarian cancer
title_sort maelstrom promotes tumor metastasis through regulation of fgfr4 and epithelial mesenchymal transition in epithelial ovarian cancer
topic Ovarian cancer
Maelstrom
EMT
Metastasis
FGFR4
url https://doi.org/10.1186/s13048-022-00992-4
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