WISP2 promotes cell proliferation via targeting ERK and YAP in ovarian cancer cells

Background Wnt-inducible signaling pathway protein 2 (WISP2) is a wnt1-induced signaling pathway protein 2. Although studies indicate that WISP2 may promote the development of various tumors, its role in ovarian cancer remains unclear. The objective of the current study was to analyze the effects of...

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Bibliographic Details
Published in:Journal of ovarian research 2020-07, Vol.13 (1), p.1-85, Article 85
Main Authors: Shi, Zi-Qing, Chen, Zi-Yan, Han, Yao, Zhu, Heng-Yan, Lyu, Meng-Dan, Zhang, Han, Zhang, Yi, Yang, Liu-Qing, Pan, Wei-Wei
Format: Article
Language:English
Subjects:
Analysis
Apoptosis
Cancer cells
Cancer therapies
CCAAT/enhancer-binding protein
Cell adhesion & migration
Cell cycle
Cell growth
Cell migration
Cell proliferation
Chemotherapy
Clonal deletion
CRISPR
Development and progression
Extracellular matrix
Extracellular signal-regulated kinase
Immunohistochemistry
Kinases
Medical prognosis
Ovarian cancer
Phosphorylation
Proliferation
Protein binding
Protein expression
Proteins
Senescence
Signal transduction
Tumor cell lines
Tumors
Western blotting
WISP2
Wnt protein
Yes-associated protein
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Summary:Background Wnt-inducible signaling pathway protein 2 (WISP2) is a wnt1-induced signaling pathway protein 2. Although studies indicate that WISP2 may promote the development of various tumors, its role in ovarian cancer remains unclear. The objective of the current study was to analyze the effects of WISP2 on the proliferation and migration of ovarian cancer cells in vitro and in vivo. Results Immunohistochemistry and western blotting indicated that WISP2 was highly expressed in various ovarian cancer tissues and cell lines, but weakly expressed in normal ovary tissue. WISP2 deletion inhibited cell growth, clone formation, and migration of ovarian cancer cells while promoting cell apoptosis and affecting the cell cycle. This growth inhibitory effect caused by WISP2 loss is due to the inhibition of phosphorylated extracellular signal-related kinase (p-ERK)1/2, as well as CCAAT/enhancer-binding protein [alpha] (CEBP[alpha]) and CEPB[beta]. In addition, WISP2 deletion also activated the Yes-associated protein (YAP). Conclusion WISP2 deletion inhibits ovarian cancer cell proliferation by affecting ERK signaling pathways. Keywords: Ovarian cancer, Proliferation, Apoptosis, WISP2
ISSN:1757-2215
1757-2215
DOI:10.1186/s13048-020-00687-8