title: Wnt5a Signaling in Cancer.
abstract: Wnt5a is involved in activating several non-canonical WNT signaling pathways, through binding to different members of the Frizzled- and Ror-family receptors. Wnt5a signaling is critical for regulating normal developmental processes, including proliferation, differentiation, migration, adhesion and polarity. However, the aberrant activation or inhibition of Wnt5a signaling is emerging as an important event in cancer progression, exerting both oncogenic and tumor suppressive effects. Recent studies show the involvement of Wnt5a in regulating cancer cell invasion, metastasis, metabolism and inflammation. In this article, we review findings regarding the molecular mechanisms and roles of Wnt5a signaling in various cancer types, and highlight Wnt5a in ovarian cancer.
authors: Integrated Biomedical Sciences Program, Department of Chemistry and Biochemistry, Harper Cancer Research Institute, University of Notre Dame, South Bend, IN 46617, USA. Marwa.S.Asem.2@nd.edu.
authors: Marwa S
authors: MS
authors: Asem
authors: Department of Applied and Computational Mathematics and Statistics, Harper Cancer Research Institute, University of Notre Dame, Notre Dame, IN 46656, USA. buechler.1@nd.edu.
authors: Steven
authors: S
authors: Buechler
authors: Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160, USA. rwates@kumc.edu.
authors: Rebecca Burkhalter
authors: RB
authors: Wates
authors: Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. miller.climb@gmail.com.
authors: Daniel L
authors: DL
authors: Miller
authors: Department of Chemistry and Biochemistry, Harper Cancer Research Institute, University of Notre Dame, South Bend, IN 46617, USA. sstack@nd.edu.
authors: M Sharon
authors: MS
authors: Stack
keywords: Wnt5a; cancer; epithelial-mesenchymal transition (EMT); frizzled (Fzd); inflammation; microenvironment; non-canonical Wnt signaling; ovarian cancer; receptor tyrosine kinase-like orphan receptor (Ror); senescence