ArticleOncotarget2017
Glucose availability controls ATF4-mediated MITF suppression to drive melanoma cell growth.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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
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Who cites it
46 citing papers in PubMed, 68 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
- Metabolic buffering restricts phenotype switching in melanoma.The EMBO journal · 2026Article
- MITF Is an Essential and Functionally Multifaceted Transcription Factor in Cutaneous Melanoma.Cancers · 2026Review
- Transcription Factor ATF4 Deletion Reprograms Glucose Metabolism in Clear Cell Renal Cell Carcinoma.Cancers · 2026Article
- AhR-dependent ferroptosis as a therapeutic opportunity to counteract BRAFi-resistance in melanoma.Cell death discovery · 2026Article
- Androgen receptor and fatty acid oxidation cooperate in ferroptosis evasion in BRAFi resistant melanoma.Cell death & disease · 2026Article
- MITF, TFEB, and TFE3 drive distinct adaptive gene expression programs and immune infiltration in melanoma.Cell reports · 2025Article
- Antagonistic roles for MITF and TFE3 in melanoma plasticity.Cell reports · 2025Article
- Acquired resistance to immune checkpoint therapy is caused by glycoprotein non-metastatic melanoma protein B signal cascade.Communications medicine · 2025Article
- High-Glucose-Induced Metabolic and Redox Alterations Are Distinctly Modulated by Various Antidiabetic Agents and Interventions Against FABP5/7, MITF and ANGPTL4 in Melanoma A375 Cells.International journal of molecular sciences · 2025Article
- DeepIMAGER: Deeply Analyzing Gene Regulatory Networks from scRNA-seq Data.Biomolecules · 2024Article
- Thiol starvation triggers melanoma state switching in an ATF4 and NRF2-dependent manner.Redox biology · 2024Article
- Significant and Various Effects of ML329-Induced MITF Suppression in the Melanoma Cell Line.Cancers · 2024Article
- Skin Cancer Microenvironment: What We Can Learn from Skin Aging?International journal of molecular sciences · 2023Review
- Neurons require glucose uptake and glycolysis in vivo.Cell reports · 2023Article
- The αMSH-Dependent PI3K Pathway Supports Energy Metabolism, via Glucose Uptake, in Melanoma Cells.Cells · 2023Article
- Phenotype Switching and the Melanoma Microenvironment; Impact on Immunotherapy and Drug Resistance.International journal of molecular sciences · 2023Review
- New Insights into the Phenotype Switching of Melanoma.Cancers · 2022Review
- Epigenetic Mechanisms Underlying Melanoma Resistance to Immune and Targeted Therapies.Cancers · 2022Review
- The MITF regulatory network in melanoma.Pigment cell & melanoma research · 2022Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
It is well know that cancer cells have adopted an altered metabolism and that glucose is a major source of energy for these cells. In melanoma, enhanced glucose usage is favoured through the hyper-activated MAPK pathway, which suppresses OXPHOS and stimulates glycolysis. However, it has not been addressed how glucose availability impacts on melanoma specific signaling pathways that drive melanoma cell proliferation. Here we show that melanoma cells are dependent on high glucose levels for efficient growth. Thereby, glucose metabolism controls the expression of the melanoma fate transcription factor MITF, a master regulator of melanoma cell survival and proliferation, invasion and therapy resistance. Restriction of glucose availability to physiological concentrations induces the production of reactive oxygen species (ROS). Increased ROS levels lead to the up-regulation of AFT4, which in turn suppresses MITF expression by competing with CREB, an otherwise potent inducer of the MITF promoter. Our data give new insight into the complex regulation of MITF, a key regulator of melanoma biology, and support previous findings that link metabolic disorders such as hyperglycemia and diabetes with increased melanoma risk.
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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.