ArticleThe Journal of investigative dermatology2013
Melanoma cell invasiveness is promoted at least in part by the epidermal growth factor-like repeats of tenascin-C.
Article in The Journal of investigative dermatology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
The trial behind it
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
25 citing papers in PubMed, 33 citations in OpenAlex.
- The aberrant migration and differentiation of neural crest cells are associated with the production of HVP in bearded chicken.Functional & integrative genomics · 2025Article
- Deciphering the Tenascin-C Nexus: A Comprehensive Review of Its Involvement in Chronic Respiratory Diseases.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025Review
- Silencing of Epidermal Growth Factor-like Domain 8 Promotes Proliferation and Cancer Aggressiveness in Human Ovarian Cancer Cells by Activating ERK/MAPK Signaling Cascades.International journal of molecular sciences · 2024Article
- Proteomic and metabolomic profiles of plasma-derived Extracellular Vesicles differentiate melanoma patients from healthy controls.Translational oncology · 2024Article
- Ectopic CH60 mediates HAPLN1-induced cell survival signaling in multiple myeloma.Life science alliance · 2023Article
- Exosomes produced by melanoma cells significantly influence the biological properties of normal and cancer-associated fibroblasts.Histochemistry and cell biology · 2022Article
- Prostate tumor-induced stromal reprogramming generates Tenascin C that promotes prostate cancer metastasis through YAP/TAZ inhibition.Oncogene · 2022Article
- Silencing Osteopontin Expression Inhibits Proliferation, Invasion and Induce Altered Protein Expression in Melanoma Cells.Pathology oncology research : POR · 2021Article
- Analysis of Melanoma Secretome for Factors That Directly Disrupt the Barrier Integrity of Brain Endothelial Cells.International journal of molecular sciences · 2020Article
- Detection and prognostic role of heterogeneous populations of melanoma circulating tumour cells.British journal of cancer · 2020Article
- Biologically Active TNIIIA2 Region in Tenascin-C Molecule: A Major Contributor to Elicit Aggressive Malignant Phenotypes From Tumors/Tumor Stroma.Frontiers in immunology · 2020Review
- Adult Stem Cell Functioning in the Tumor Micro-Environment.International journal of molecular sciences · 2019Review
- The great escape: How metastases of melanoma, and other carcinomas, avoid elimination.Experimental biology and medicine (Maywood, N.J.) · 2018Review
- The Pro-reparative Engine: Stem Cells Aid Healing by Dampening Inflammation.Current pathobiology reports · 2018Article
- Tyro3-mediated phosphorylation of ACTN4 at tyrosines is FAK-dependent and decreases susceptibility to cleavage by m-Calpain.The international journal of biochemistry & cell biology · 2018Article
- Bi-directional exosome-driven intercommunication between the hepatic niche and cancer cells.Molecular cancer · 2017Article
- Article
- Liver metastases: Microenvironments and ex-vivo models.Experimental biology and medicine (Maywood, N.J.) · 2016Review
- Tenascin-C Signaling in melanoma.Cell adhesion & migration · 2015Review
- Tenascin C in metastasis: A view from the invasive front.Cell adhesion & migration · 2015Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Tenascin-C (TNC), overexpressed in invasive growths, has been implicated in progression of melanoma, but the source and function of this molecule are not well defined. We found TNC expression at the front of invading melanoma cells, and that adding TNC to matrices enhances individual melanoma cell migration. As TNC is a multidomain protein, we examined the role of the TNC EGF-like (EGFL) repeats as these activate motogenic signaling cascades. We overexpressed a TNC fragment containing the assembly and EGFL domains of TNC (TNCEGFL). TNCEGFL-expressing melanoma cells had lower speed and persistence in 2D migration assays due to a shift in the adhesion-contractility balance, as expression of TNCEGFL delayed melanoma cell attachment and spreading. The less adhesive phenotype was due, in part, to increased Rho-associated kinase (ROCK) signaling concomitant with myosin light chain 2 and MYPT phosphorylation. Inhibition of ROCK activity, which drives transcellular contractility, restored adhesion of TNCEGFL-expressing melanoma cells and increased their migration in 2D. In contrast to the diminished migration in 2D, TNCEGFL-expressing melanoma cells had higher invasive potential in Matrigel invasion assays, with cells expressing TNCEGFL having amoeboid morphology. Our findings suggest that melanoma-derived TNCEGFL exert a role in melanoma invasion by modulating ROCK signaling and cell migration.
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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.