ArticleThe Journal of cell biology2005
MITF links differentiation with cell cycle arrest in melanocytes by transcriptional activation of INK4A.
Article in The Journal of cell biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.
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Who cites it
102 citing papers in PubMed, 257 citations in OpenAlex.
- MITF-Driven melanoma plasticity as a core mechanism of therapy resistance: integrating microenvironmental signaling, mechanotransduction, and metabolic reprogramming.Cell cycle (Georgetown, Tex.) · 2026Review
- MITF Is an Essential and Functionally Multifaceted Transcription Factor in Cutaneous Melanoma.Cancers · 2026Review
- MITF, TFEB, and TFE3 drive distinct adaptive gene expression programs and immune infiltration in melanoma.Cell reports · 2025Article
- GATA6 in pancreatic cancer initiation and progression.Genes & diseases · 2025Review
- Amelanotic Melanoma-Biochemical and Molecular Induction Pathways.International journal of molecular sciences · 2024Review
- DNA damage remodels the MITF interactome to increase melanoma genomic instability.Genes & development · 2024Article
- Mechanisms of Melanoma Progression and Treatment Resistance: Role of Cancer Stem-like Cells.Cancers · 2024Review
- Identification of BRAF, CCND1, and MYC mutations in a patient with multiple primary malignant tumors: a case report and review of the literature.World journal of surgical oncology · 2023Review
- An adverse tumor-protective effect of IDO1 inhibition.Cell reports. Medicine · 2023Article
- A unique hyperdynamic dimer interface permits small molecule perturbation of the melanoma oncoprotein MITF for melanoma therapy.Cell research · 2023Article
- The MITF regulatory network in melanoma.Pigment cell & melanoma research · 2022Article
- DUSP4 protects BRAF- and NRAS-mutant melanoma from oncogene overdose through modulation of MITF.Life science alliance · 2022Article
- MITF in Normal Melanocytes, Cutaneous and Uveal Melanoma: A Delicate Balance.International journal of molecular sciences · 2022Review
- Uveal Melanoma Cell Line Proliferation Is Inhibited by Ricolinostat, a Histone Deacetylase Inhibitor.Cancers · 2022Article
- Signal pathways of melanoma and targeted therapy.Signal transduction and targeted therapy · 2021Review
- Loss of Melanopsin (OPN4) Leads to a Faster Cell Cycle Progression and Growth in Murine Melanocytes.Current issues in molecular biology · 2021Article
- Modulating skin colour: role of the thioredoxin and glutathione systems in regulating melanogenesis.Bioscience reports · 2021Review
- How Neural Crest Transcription Factors Contribute to Melanoma Heterogeneity, Cellular Plasticity, and Treatment Resistance.International journal of molecular sciences · 2021Review
- MITF is a driver oncogene and potential therapeutic target in kidney angiomyolipoma tumors through transcriptional regulation of CYR61.Oncogene · 2021Article
- The Impact of Hyaluronan on Tumor Progression in Cutaneous Melanoma.Frontiers in oncology · 2021Review
42 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Cell cycle exit is required for proper differentiation in most cells and is critical for normal development, tissue homeostasis, and tumor suppression. However, the mechanisms that link cell cycle exit with differentiation remain poorly understood. Here, we show that the master melanocyte differentiation factor, microphthalmia transcription factor (MITF), regulates cell cycle exit by activating the cell cycle inhibitor INK4A, a tumor suppressor that frequently is mutated in melanomas. MITF binds the INK4A promoter, activates p16(Ink4a) mRNA and protein expression, and induces retinoblastoma protein hypophosphorylation, thereby triggering cell cycle arrest. This activation of INK4A was required for efficient melanocyte differentiation. Interestingly, MITF was also required for maintaining INK4A expression in mature melanocytes, creating a selective pressure to escape growth inhibition by inactivating INK4A. These findings demonstrate that INK4A can be regulated by a differentiation factor, establish a mechanistic link between melanocyte differentiation and cell cycle exit, and potentially explain the tissue-specific tendency for INK4A mutations to occur in 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.