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Related Experiment Video

Updated: Jan 30, 2026

The Three-Dimensional Human Skin Reconstruct Model: a Tool to Study Normal Skin and Melanoma Progression
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KLF9-dependent ROS regulate melanoma progression in stage-specific manner.

Archis Bagati1,2, Sudha Moparthy1, Emily E Fink1

  • 1Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY, USA.

Oncogene
|January 22, 2019
PubMed
Summary
This summary is machine-generated.

Klf9 deficiency suppresses premalignant melanoma growth by regulating reactive oxygen species (ROS). However, Klf9 is not essential for primary melanoma formation but promotes metastasis. Topical antioxidants may suppress premalignant melanoma growth.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Dermatology

Background:

  • The role of reactive oxygen species (ROS) in melanoma progression is debated, with antioxidants promoting metastasis but their role in earlier stages unclear.
  • Genes regulating ROS require functional characterization across all cancer progression stages in mouse models.
  • Klf9, a transcriptional regulator of oxidative stress, has not been studied in the context of melanoma progression.

Purpose of the Study:

  • To investigate the role of Klf9 and ROS in different stages of melanoma progression using mouse models.
  • To determine the functional characterization of Klf9-dependent ROS in melanoma development.
  • To explore the therapeutic potential of targeting Klf9-dependent ROS in premalignant melanocytes.

Main Methods:

  • Crossed Klf9 knockout mice with BrafCA (premalignant hyperplasia) and BrafCA/Pten-/- (primary melanoma and metastasis) conditional melanocytic mouse models.
  • Assessed the impact of Klf9 deficiency on melanocytic hyperplasia, primary tumor formation, growth, and metastasis.
  • Treated mice with N-acetyl cysteine (antioxidant) to mimic Klf9 deficiency effects.
  • Investigated the mechanistic link between BRAFV600E, KLF9, ROS, and ERK1/2 signaling pathways.

Main Results:

  • Klf9 deficiency inhibited premalignant melanocytic hyperplasia in BrafCA mice.
  • Klf9 deficiency did not affect primary melanoma formation or growth in BrafCA/Pten-/- mice but promoted metastasis.
  • N-acetyl cysteine treatment phenocopied Klf9 deficiency, suppressing melanocytic hyperplasia.
  • BRAFV600E upregulated KLF9, and KLF9-dependent ROS were crucial for ERK1/2 activation and proliferation in premalignant cells.
  • PTEN loss rendered melanomas insensitive to KLF9 and ROS, despite continued ERK1/2 activation.

Conclusions:

  • Klf9 plays an essential role in BRAFV600E signaling in premalignant melanocytes via KLF9-dependent ROS.
  • ROS have a variable role in premalignant versus transformed melanocytic cells.
  • Targeting Klf9-dependent ROS may offer a novel strategy for suppressing premalignant melanoma growth, potentially through topical antioxidants.