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<p>High salt diet (HSD) is known to reduce cancer growth in some tumor models, which has been attributed to tissue accumulation of sodium that enhances local anti-tumor immunity. Here, we show that a HSD inhibits melanoma growth independent of sodium accumulation and immune cells in skin and lung. Melanoma cells from mice on a HSD upregulated the metabolic inhibitor Tuberous sclerosis complex 2 (TSC2), causing metabolic shutdown despite nutrient availability. Furthermore, Microphthalmia-associated transcription factor (MITF), a crucial regulator of melanoma metabolism and differentiation, was upregulated, resulting in enhanced melanogenesis and cell cycle arrest. Thus, a HSD reversed the de-differentiation of melanoma cells and promoted their re-differentiation into a “normal” melanocytic state. These findings suggest that the anti-tumor effect of HSD may be tumor-specific and in some cases immune cell-independent.</p>

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High-salt diet induces immune-independent re-differentiation, metabolic shut down and cell cycle arrest of melanoma

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月20日

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  • Clivia Lisowski,
  • Natascha E. Stumpf,
  • Katarzyna Jobin,
  • Daniela Klaus,
  • Melanie Eichler,
  • Ann-Kathrin Baumgart,
  • Olena Babyak,
  • Mirjam Meißner,
  • Agnes Schröder,
  • Patrick Neubert,
  • Vanessa Schmitt,
  • Marcel Michla,
  • Süleyman Bozkurt,
  • Jelena Zurkovic,
  • Daniel Hinze,
  • Jana Liebing,
  • Matthias Eckhardt,
  • Christoph Heuser,
  • Lea Seep,
  • Annkristin Heine,
  • Janine Becker-Gotot,
  • Christoph Thiele,
  • Christian Münch,
  • Thomas Becker,
  • Jonathan Jantsch,
  • Christoph Wilhelm,
  • Michael Hölzel,
  • Christian Kurts

摘要

High salt diet (HSD) is known to reduce cancer growth in some tumor models, which has been attributed to tissue accumulation of sodium that enhances local anti-tumor immunity. Here, we show that a HSD inhibits melanoma growth independent of sodium accumulation and immune cells in skin and lung. Melanoma cells from mice on a HSD upregulated the metabolic inhibitor Tuberous sclerosis complex 2 (TSC2), causing metabolic shutdown despite nutrient availability. Furthermore, Microphthalmia-associated transcription factor (MITF), a crucial regulator of melanoma metabolism and differentiation, was upregulated, resulting in enhanced melanogenesis and cell cycle arrest. Thus, a HSD reversed the de-differentiation of melanoma cells and promoted their re-differentiation into a “normal” melanocytic state. These findings suggest that the anti-tumor effect of HSD may be tumor-specific and in some cases immune cell-independent.