ArticleBritish journal of cancer1998
Regulation of Wnt5a expression in human mammary cells by protein kinase C activity and the cytoskeleton.
Article in British journal of cancer, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 44 citations in OpenAlex.
- Cdk7 promotes neuritogenesis in cortical neurons and contributes to social behavior in mice.Cellular and molecular life sciences : CMLS · 2026Article
- Wnt2b and Wnt5a expression is highly associated with M2 TAMs in non‑small cell lung cancer.Oncology reports · 2022Article
- The Pathogenic Role of Smooth Muscle Cell-Derived Wnt5a in a Murine Model of Lung Fibrosis.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Non-canonical WNT5a regulates Epithelial-to-Mesenchymal Transition in the mouse ovarian surface epithelium.Scientific reports · 2020Article
- Multiple Roles of WNT5A in Breast Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2016Review
- Gene expression analyses of primary melanomas reveal CTHRC1 as an important player in melanoma progression.Oncotarget · 2016Article
- WNT5A promotes stemness characteristics in nasopharyngeal carcinoma cells leading to metastasis and tumorigenesis.Oncotarget · 2015Article
- Wnt5a/β-catenin signaling drives calcium-induced differentiation of human primary keratinocytes.The Journal of investigative dermatology · 2014Article
- MicroRNA-200b suppresses arsenic-transformed cell migration by targeting protein kinase Cα and Wnt5b-protein kinase Cα positive feedback loop and inhibiting Rac1 activation.The Journal of biological chemistry · 2014Article
- Striking the target in Wnt-y conditions: intervening in Wnt signaling during cancer progression.Biochemical pharmacology · 2010Review
- The orphan tyrosine kinase receptor, ROR2, mediates Wnt5A signaling in metastatic melanoma.Oncogene · 2010Article
- Hear the Wnt Ror: how melanoma cells adjust to changes in Wnt.Pigment cell & melanoma research · 2009Review
- Heparan sulfate proteoglycan modulation of Wnt5A signal transduction in metastatic melanoma cells.The Journal of biological chemistry · 2009Article
- The Wnt5A/protein kinase C pathway mediates motility in melanoma cells via the inhibition of metastasis suppressors and initiation of an epithelial to mesenchymal transition.The Journal of biological chemistry · 2007Article
- Wnt11 signaling promotes proliferation, transformation, and migration of IEC6 intestinal epithelial cells.The Journal of biological chemistry · 2004Article
- Functional development of the mammary gland: use of expression profiling and trajectory clustering to reveal changes in gene expression during pregnancy, lactation, and involution.Journal of mammary gland biology and neoplasia · 2003Article
- Understanding signaling cascades in melanoma.Photochemistry and photobiologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Wnts can be classified into two classes based on their ability to transform cells. The Wnt5a class can antagonize the effects of transforming Wnts partly through effects on cell migration. To understand the mechanisms of regulation of Wnt5a, we investigated its expression in human normal and breast cancer cell lines. Elevation of Wnt5a in HB2, a normal breast epithelial cell line, was linearly correlated with cell density, but this did not occur in cancer cell lines. We examined intracellular events responsible for the regulation of Wnt5a by cell to cell contacts, using various metabolic agents known to affect signal transduction pathways. Agents that selectively blocked protein kinase C (calphostin C) or protein tyrosine kinases (genistein) reduced the level of Wnt5a expression markedly. Protein kinase C activation by phorbol 12-myristate 13-acetate up-regulated Wnt5a partly through prolongation of Wnt5a mRNA half-life. Cytoskeleton reorganization following cytochalasin D treatment caused an induction of Wnt5a, which was associated with changes in cell morphology. Calphostin C did not block these effects, showing that protein kinase C is acting upstream of cytoskeletal modulation. However, the cancer cell lines treated with cytochalasin D showed no changes in cell morphology or Wnt5a induction, suggesting disruption of this regulatory pathway in cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.