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Author Spotlight: Recreating Melanoma Complexity with Patient-Derived Organoids for Immunotherapy Evaluation
Published on: September 6, 2024
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Metabolic flexibility in melanoma: A potential therapeutic target
Maria Rosaria Ruocco1, Angelica Avagliano2, Giuseppina Granato3
1Department of Molecular Medicine and Medical Biotechnology, University of Naples Federico II, Naples, Italy.
Seminars in Cancer Biology
|July 31, 2019
Summary
Cutaneous melanoma (CM) cells exhibit metabolic plasticity, relying on glycolysis for energy. This metabolic adaptability drives BRAF/MEK inhibitor resistance and impacts the tumor microenvironment and immune response.
Area of Science:
- Oncology
- Cancer Metabolism
- Molecular Biology
Background:
- Cutaneous melanoma (CM) is a highly metastatic and drug-resistant cancer.
- CM exhibits significant metabolic plasticity, linking oncogenic activation to energy metabolism.
- Melanoma cells utilize both cytosolic and mitochondrial pathways for ATP production, with glycolysis being crucial.
Purpose of the Study:
- To review the regulation of metabolic alterations in melanoma.
- To explore metabolic interactions between melanoma cells and the tumor microenvironment.
- To summarize melanoma therapies, focusing on BRAF/MEK targeted therapy and resistance mechanisms.
Main Methods:
- Literature review of scientific articles on melanoma metabolism, oncogenic signaling, and therapy resistance.
- Analysis of the interplay between cellular metabolism, tumor microenvironment, and immune response in CM.
- Synthesis of current knowledge on BRAF/MEK pathway targeted therapies and associated resistance.
Main Results:
- Melanoma's high energy demand is met by upregulated glycolysis, linked to BRAFV600E mutations.
- Melanoma's metabolic plasticity contributes to resistance against BRAF/MEK inhibitors (BRAFi/MEKi).
- Metabolic interactions between melanoma and its microenvironment influence immune evasion and tumor progression.
Conclusions:
- Understanding melanoma's metabolic reprogramming is key to developing effective therapies.
- Targeting metabolic pathways may overcome resistance to BRAF/MEK inhibitors.
- The tumor microenvironment significantly modulates melanoma's metabolic landscape and therapeutic response.
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