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Tacrolimus and ascomycin inhibit melanoma cell growth, migration and invasion via targeting nuclear factor of

Tian Xiao1, Wencong Chen1, Shuangfeng Wang1

  • 1Guangdong Key Laboratory for Genome Stability and Disease Prevention, Shenzhen Key Laboratory of Translational Medicine of Tumor, Carson International Cancer Center and Department of Cell Biology and Genetics, Shenzhen University School of Medicine.

Melanoma Research
|April 18, 2020
PubMed

Insights

Nuclear factor of activated T-cells 3 (NFAT3) drives melanoma growth. Inhibiting NFAT3 with calcineurin inhibitors like tacrolimus (FK506) reduces melanoma cell migration, invasion, and proliferation, offering potential new treatments.

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Melanoma is an aggressive skin cancer with high metastatic potential.
  • Nuclear factor of activated T-cells (NFATs) are key immune response regulators.
  • NFAT3, unlike other NFATs, is not found in immune cells, and its role in cancer is debated, though previously linked to melanoma survival and growth.

Purpose of the Study:

  • To investigate the role of NFAT3 in melanoma cell behavior.
  • To determine the effect of calcineurin (CaN) inhibitors on melanoma progression.
  • To elucidate the mechanism by which CaN inhibitors impact melanoma.

Main Methods:

  • Knockdown of NFAT3 expression in melanoma cells.
  • Treatment of melanoma cells with calcineurin inhibitors tacrolimus (FK506) and ascomycin (FK520).
  • Assessment of cell migration, invasion, proliferation, and colony formation.
  • Analysis of NFAT3 nuclear translocation and transcriptional activity.

Main Results:

  • NFAT3 knockdown inhibited melanoma cell migration, invasion, proliferation, and colony formation.
  • FK506 and FK520 treatment similarly inhibited these melanoma cell behaviors.
  • Mechanistic studies showed FK506 and FK520 block NFAT3 nuclear translocation and reduce its transcriptional activity.

Conclusions:

  • The antimelanoma effects of FK506 and FK520 are partly mediated by inhibiting the oncogenic factor NFAT3.
  • Inhibiting NFAT3 may represent a viable therapeutic strategy for clinical melanoma treatment.

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