ArticleJournal of experimental & clinical cancer research : CR2016
WNT5A signaling impairs breast cancer cell migration and invasion via mechanisms independent of the epithelial-mesenchymal transition.
Article in Journal of experimental & clinical cancer research : CR, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 64 citations in OpenAlex.
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- Wnt5a augments intracellular free cholesterol levels and promotes castration resistance in prostate cancer.Journal of translational medicine · 2025Article
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- Differential expression of WNT5A long and short isoforms in non-muscle-invasive bladder urothelial carcinoma.Histology and histopathology · 2024Article
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- β-catenin inhibitors in cancer therapeutics: intricacies and way forward.Bioengineered · 2023Review
- ST6GALNAC1 promotes the invasion and migration of breast cancer cells via the EMT pathway.Genes & genomics · 2023Article
- Organotypic 3D Cell-Architecture Impacts the Expression Pattern of miRNAs-mRNAs Network in Breast Cancer SKBR3 Cells.Non-coding RNA · 2023Article
- TCAF2 in Pericytes Promotes Colorectal Cancer Liver Metastasis via Inhibiting Cold-Sensing TRPM8 Channel.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Non-canonical WNT5A-ROR signaling: New perspectives on an ancient developmental pathway.Current topics in developmental biology · 2023Article
- NTF4 plays a dual role in breast cancer in mammary tumorigenesis and metastatic progression.International journal of biological sciences · 2023Article
- Identification of molecularly unique tumor-associated mesenchymal stromal cells in breast cancer patients.PloS one · 2023Article
- Integration of multi-omics data reveals a novel hybrid breast cancer subtype and its biomarkers.Frontiers in oncology · 2023Article
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWNT5A (-/-) mammary tissue has been shown to exhibit increased ductal elongation, suggesting elevated mammary cell migration. Increased epithelial cell migration/invasion has often but not always been linked to the epithelial-mesenchymal transition (EMT). In the current study, we investigated the loss of WNT5A in HB2 human mammary epithelial cells and hypothesized that this loss increased their invasion via the EMT. Based on these results, we postulated that suppression of breast cancer cell migration and invasion by WNT5A is due to EMT reversal.
methodsWNT5A was transiently knocked down using specific siRNAs, whereas WNT5A signaling was induced in MDA-MB468 and MDA-MB231 breast cancer cells by stably transfecting cells with WNT5A or treating them with recombinant WNT5A (rWNT5A). Changes in EMT markers, CD44, pAKT and AKT expression were assessed using Western blotting and immunofluorescence. The physiological relevance of altered WNT5A signaling was assessed using migration and invasion assays.
resultsWNT5A knockdown in HB2 mammary epithelial cells resulted in EMT-like changes and increased invasiveness, and these changes were partially reversed by the addition of rWNT5A. These data suggest that WNT5A might inhibit breast cancer cell migration and invasion by a similar EMT reversal. Contrary to our expectations, we did not observe any changes in the EMT status of breast cancer cells, either after treatment with rWNT5A or stable transfection with a WNT5A plasmid, despite the parallel WNT5A-induced inhibition of migration and invasion. Instead, we found that WNT5A signaling impaired CD44 expression and its downstream signaling via AKT. Moreover, knocking down CD44 in breast cancer cells using siRNA impaired cell migration and invasion.
conclusionsWNT5A bi-directionally regulates EMT in mammary epithelial cells, thereby affecting their migration and invasion. However, the ability of WNT5A to inhibit breast cancer cell migration and invasion is an EMT-independent mechanism that, at least in part, can be explained by decreased CD44 expression.
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