ArticleThe Journal of investigative dermatology2012
GSK3β inhibition blocks melanoma cell/host interactions by downregulating N-cadherin expression and decreasing FAK phosphorylation.
Article in The Journal of investigative dermatology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- Diabetes mellitus is associated with earlier detection of posterior uveal melanoma.European journal of ophthalmology · 2026Article
- Apoptosis, Cell Growth, and Glycogen Synthase Kinase 3β Phosphorylation in Caffeic Acid-Treated Human Malignant Melanoma Cells.Biomedicines · 2025Article
- YAP1 controls the N-cadherin-mediated tumor-stroma interaction in melanoma progression.Research square · 2023Article
- Phytochemical Analysis, In Vitro Biological Activities, and Computer-Aided Analysis ofMolecules (Basel, Switzerland) · 2023Article
- Canonical Wnt and TGF-β/BMP signaling enhance melanocyte regeneration but suppress invasiveness, migration, and proliferation of melanoma cells.Frontiers in cell and developmental biology · 2023Article
- NUMB as a Therapeutic Target for Melanoma.The Journal of investigative dermatology · 2022Article
- Cocktail ofFrontiers in pharmacology · 2022Article
- Review
- Potential Health Benefits Associated with Lunasin Concentration in Dietary Supplements and Lunasin-Enriched Soy Extract.Nutrients · 2021Article
- Arginine deprivation inhibits pancreatic cancer cell migration, invasion and EMT via the down regulation of Snail, Slug, Twist, and MMP1/9.Journal of physiology and biochemistry · 2020Article
- RETRACTED: GSK-3β-Targeting Fisetin Promotes Melanogenesis in B16F10 Melanoma Cells and Zebrafish Larvae through β-Catenin Activation.International journal of molecular sciences · 2020Article
- Article
- Roles of GSK-3 and microRNAs on epithelial mesenchymal transition and cancer stem cells.Oncotarget · 2017Review
- A large-scale RNAi screen identifies LCMR1 as a critical regulator of Tspan8-mediated melanoma invasion.Oncogene · 2017Article
- Interleukin-32α induces migration of human melanoma cells through downregulation of E-cadherin.Oncotarget · 2016Article
- Analysis of epithelial-mesenchymal transition markers in psoriatic epidermal keratinocytes.Open biology · 2015Article
- Ligand-independent EPHA2 signaling drives the adoption of a targeted therapy-mediated metastatic melanoma phenotype.Cancer discovery · 2015Article
- Focal adhesion kinase-mediated activation of glycogen synthase kinase 3β regulates IL-33 receptor internalization and IL-33 signaling.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Phosphoproteomic analysis of basal and therapy-induced adaptive signaling networks in BRAF and NRAS mutant melanoma.Proteomics · 2015Article
- GSK3β controls epithelial-mesenchymal transition and tumor metastasis by CHIP-mediated degradation of Slug.Oncogene · 2014Article
Corrections and comments
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Authors and funding
15 authors at 8 institutions in 2 countries.
Funding
Abstract
This study addresses the role of glycogen synthase kinase (GSK)-3β signaling in the tumorigenic behavior of melanoma. Immunohistochemical staining revealed GSK3β to be focally expressed in the invasive portions of 12 and 33% of primary and metastatic melanomas, respectively. GSK3 inhibitors and small interfering RNA (siRNA) knockdown of GSK3β were found to inhibit the motile behavior of melanoma cells in scratch wound, three-dimensional collagen-implanted spheroid, and modified Boyden chamber assays. Functionally, inhibition of GSK3β signaling was found to suppress N-cadherin expression at the messenger RNA and protein levels, and was associated with decreased expression of the transcription factor Slug. Pharmacological and genetic ablation of GSK3β signaling inhibited the adhesion of melanoma cells to both endothelial cells and fibroblasts and prevented transendothelial migration, an effect rescued by the forced overexpression of N-cadherin. A further role for GSK3β signaling in invasion was suggested by the ability of GSK3β inhibitors and siRNA knockdown to block phosphorylation of focal adhesion kinase (FAK) and increase the size of focal adhesions. In summary, we have, to our knowledge, demonstrated a previously unreported role for GSK3β in modulating the motile and invasive behavior of melanoma cells through N-cadherin and FAK. These studies suggest the potential therapeutic utility of inhibiting GSK3β in defined subsets of melanoma.
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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.