ArticleScientific reports2020
SPOCK1 is a novel inducer of epithelial to mesenchymal transition in drug-induced gingival overgrowth.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Mechanobiology of Matricellular Proteins in Bladder Cancer: A Narrative Review and Bioinformatics Analysis.Biomolecules · 2026Review
- SPARC family proteins: matricellular modulators of cancer progression and therapeutic resistance.Cancer gene therapy · 2026Review
- SPOCK1 overexpression suggests poor prognosis in head and neck squamous cell carcinomas.Pathology oncology research : POR · 2026Article
- The functional role of the extracellular matrix in inflammatory bowel disease associated gut fibrosis.Matrix biology : journal of the International Society for Matrix Biology · 2025Review
- CHD1L in cancer and beyond: structure, oncogenic functions, and therapeutic potential.Journal of experimental & clinical cancer research : CR · 2025Review
- CellPie: a scalable spatial transcriptomics factor discovery method via joint non-negative matrix factorization.Nucleic acids research · 2025Article
- SPOCK1, as a potential prognostic and therapeutic biomarker for lung adenocarcinoma, is associated with epithelial-mesenchymal transition and immune evasion.Journal of translational medicine · 2023Article
- Diverse activity of miR-150 in Tumor development: shedding light on the potential mechanisms.Cancer cell international · 2023Review
- Derivation of Human Extraembryonic Mesoderm-like Cells from Primitive Endoderm.International journal of molecular sciences · 2023Article
- Adjustable extracellular matrix rigidity tumor model for studying stiffness dependent pancreatic ductal adenocarcinomas progression and tumor immunosuppression.Bioengineering & translational medicine · 2023Article
- Drug-Induced Gingival Overgrowth-Molecular Aspects of Drug Actions.International journal of molecular sciences · 2023Review
- Epithelial-to-mesenchymal transition, inflammation, subsequent collagen production, and reduced proteinase expression cooperatively contribute to cyclosporin-A-induced gingival overgrowth development.Frontiers in physiology · 2023Article
- Integrating RNA-sequencing and network analysis to explore the mechanism of topical Pien Tze Huang treatment on diabetic wounds.Frontiers in pharmacology · 2023Article
- Pathogenesis of periodontitis - A potential role for epithelial-mesenchymal transition.The Japanese dental science review · 2022Review
- Serglycin Is Involved in TGF-β Induced Epithelial-Mesenchymal Transition and Is Highly Expressed by Immune Cells in Breast Cancer Tissue.Frontiers in oncology · 2022Article
- The Central Region of Testican-2 Forms a Compact Core and Promotes Cell Migration.International journal of molecular sciences · 2020Article
- Nuclear receptor 4A1 (NR4A1) upregulated by n-butylidenephthalide via the mitogen-activated protein kinase (MAPK) pathway ameliorates drug-induced gingival enlargement.BioFactors (Oxford, England)Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Few studies have investigated the role of extracellular-matrix proteoglycans in the pathogenesis of drug-induced gingival overgrowth (DIGO). SPOCK1 is an extracellular proteoglycan that induces epithelial to mesenchymal transition (EMT) in several cancer cell lines and exhibits protease-inhibitory activity. However, the role of SPOCK1 in non-cancerous diseases such as DIGO has not been well-addressed. We demonstrated that the expression of SPOCK1, TGF-β1, and MMP-9 in calcium channel blocker-induced gingival overgrowth is higher than that in non-overgrowth tissues. Transgenic mice overexpressing Spock1 developed obvious gingival-overgrowth and fibrosis phenotypes, and positively correlated with EMT-like changes. Furthermore, in vitro data indicated a tri-directional interaction between SPOCK1, TGF-β1, and MMP-9 that led to gingival overgrowth. Our study shows that SPOCK1 up-regulation in a noncancerous disease and SPOCK1-induced EMT in gingival overgrowth occurs via cooperation and crosstalk between several potential signaling pathways. Therefore, SPOCK1 is a novel therapeutic target for gingival overgrowth and its expression is a potential risk of EMT induction in cancerous lesions.
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