ArticleEMBO reports2025
Melanocyte differentiation and mechanosensation are differentially modulated by distinct extracellular matrix proteins.
Article in EMBO reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- MITF-Driven melanoma plasticity as a core mechanism of therapy resistance: integrating microenvironmental signaling, mechanotransduction, and metabolic reprogramming.Cell cycle (Georgetown, Tex.) · 2026Review
- Article
- Micropillar Topography Regulates Morphology and Melanogenesis in Melanoma Cells.Journal of functional biomaterials · 2026Article
- Aberrant laminin signaling drives melanocyte dedifferentiation and unveils a tractable therapeutic target in vitiligo.Nature communications · 2026Article
- Mitfa-Independent Melanocyte Progenitors are Highly Susceptible to GNAQ-induced Uveal Melanoma in Adult Zebrafish.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Melanocyte dysfunctions can lead to pigmentation disorders or melanoma. Melanocytes interact context-dependently with various types of ECM, including collagens and fibronectin. Alterations in ECM composition and stiffness can impact cell behavior, but their specific roles for melanocyte functions remain unclear. We here exposed melanocytes to different ECM proteins and varying substrate stiffnesses, and identified MITF, a key regulator of melanocyte differentiation and function, as an ECM- and mechanosensitive transcription factor. Moreover, distinct ECM proteins and substrate stiffness engaged a FAK/MEK/ERK/MITF signaling axis to control melanocyte functions. Collagen I restricted FAK and ERK activation, promoting elevated nuclear MITF levels, melanocyte proliferation and a differentiated transcriptomic signature. Conversely, fibronectin elicited FAK and ERK activation, reduced nuclear MITF, increased motility and a dedifferentiated transcriptomic signature. On fibronectin, inhibiting MEK/ERK activity caused increased MITF nuclear localization and enhanced melanogenesis. Additionally, FAK inhibition reduced ERK activation and enhanced melanogenesis, supporting that FAK acts upstream of ERK. Finally, melanocytes show ECM-dependent mechanoresponses. In summary, extrinsic cues exert substantial effects on melanocyte function, involving ERK-dependent MITF regulation.
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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.