ArticleAnnals of surgery2019
The Barrier Molecules Junction Plakoglobin, Filaggrin, and Dystonin Play Roles in Melanoma Growth and Angiogenesis.
Article in Annals of surgery, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Filaggrin as a potential biomarker in gastric cancer: insights from multi-omics analysis and experimental validation.Frontiers in immunology · 2026Article
- POFUT2 Mediated Fucosylation of JUP Enhances VEGFA Expression to Promote Angiogenesis in Colorectal Cancer.International journal of medical sciences · 2026Article
- FilaggrinFrontiers in genetics · 2025Article
- Functional Analysis of Membrane-Associated Scaffolding Tight Junction (TJ) Proteins in Tumorigenic Characteristics of B16-F10 Mouse Melanoma Cells.International journal of molecular sciences · 2024Article
- Clinical assessment and transcriptome analysis of host immune responses in a vaccination-challenge study using a glycoprotein G deletion mutant vaccine strain of infectious laryngotracheitis virus.Frontiers in immunology · 2024Article
- miR-195-5p as Regulator of γ-Catenin and Desmosome Junctions in Colorectal Cancer.International journal of molecular sciences · 2023Article
- Two-Dimensional Polyacrylamide Gel Electrophoresis Coupled with Nanoliquid Chromatography-Tandem Mass Spectrometry-Based Identification of Differentially Expressed Proteins and Tumorigenic Pathways in the MCF7 Breast Cancer Cell Line Transfected for Jumping Translocation Breakpoint Protein Overexpression.International journal of molecular sciences · 2023Article
- Barriers to immune cell infiltration in tumors.Journal for immunotherapy of cancer · 2023Review
- RNA-seq and ChIP-seq Identification of Unique and Overlapping Targets of GLI Transcription Factors in Melanoma Cell Lines.Cancers · 2022Article
- Activation of Oncogenic and Immune-Response Pathways Is Linked to Disease-Specific Survival in Merkel Cell Carcinoma.Cancers · 2022Article
- Identification of Core Genes and Pathways in Melanoma Metastasis via Bioinformatics Analysis.International journal of molecular sciences · 2022Article
- TMT-Based Quantitative Proteomic Analysis Reveals the Effect of Bone Marrow Derived Mesenchymal Stem Cell on Hair Follicle Regeneration.Frontiers in pharmacology · 2021Article
- Enhancer RNA SLIT2 Inhibits Bone Metastasis of Breast Cancer Through Regulating P38 MAPK/c-Fos Signaling Pathway.Frontiers in oncology · 2021Article
- Identification of Prognostic Genes in Neuroblastoma in Children by Weighted Gene Coexpression Network Analysis.Biochemistry research international · 2021Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveTo understand role of barrier molecules in melanomas.
backgroundWe have reported poor patient survival and low immune infiltration of melanomas that overexpress a set of genes that include filaggrin (FLG), dystonin (DST), junction plakoglobin (JUP), and plakophilin-3 (PKP3), and are involved in cell-cell adhesions. We hypothesized that these associations are causal, either by interfering with immune cell infiltration or by enhancing melanoma cell growth.
methodsFLG and DST were knocked out by CRISPR/Cas9 in human DM93 and murine B16-F1 melanoma cells. PKP3 and JUP were overexpressed in murine B16-AAD and human VMM39 melanoma cells by lentiviral transduction. These cell lines were evaluated in vitro for cell proliferation and in vivo for tumor burden, immune composition, cytokine expression, and vascularity.
resultsImmune infiltrates were not altered by these genes. FLG/DST knockout reduced proliferation of human DM93 melanoma in vitro, and decreased B16-F1 tumor burden in vivo. Overexpression of JUP, but not PKP3, in B16-AAD significantly increased tumor burden, increased VEGF-A, reduced IL-33, and enhanced vascularity.
conclusionsFLG and DST support melanoma cell growth in vitro and in vivo. Growth effects of JUP were only evident in vivo, and may be mediated, in part, by enhancing angiogenesis. In addition, growth-promoting effects of FLG and DST in vitro suggest that these genes may also support melanoma cell proliferation through angiogenesis-independent pathways. These findings identify FLG, DST, and JUP as novel therapeutic targets whose down-regulation may provide clinical benefit to patients with melanoma.
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