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Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate (DMBA-TPA)
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Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate (DMBA-TPA)

Published on: December 19, 2019

Modulation of epidermal tumor development caused by targeted overexpression of epidermis-type 12S-lipoxygenase

Karsten Müller1, Malte Siebert, Markus Heidt

  • 1Deutsches Krebsforschungszentrum, Research Program on Tumor Cell Regulation, 69120 Heidelberg, Germany.

Cancer Research
|August 17, 2002
PubMed

Insights

Epidermis-type 12S-lipoxygenase (LOX) may have antitumorigenic effects. Its expression level influences skin tumor development, with different LOX products playing opposing roles in carcinogenesis.

Area of Science:

  • Biochemistry
  • Dermatology
  • Oncology

Background:

  • Epidermis-type 12S-lipoxygenase (e12S-LOX) is downregulated during mouse skin tumor development.
  • This suggests a potential antitumorigenic role for e12S-LOX.
  • Understanding LOX isoform roles is crucial for skin cancer research.

Purpose of the Study:

  • To investigate the role of e12S-LOX in skin carcinogenesis.
  • To determine the impact of differential e12S-LOX expression on tumor development.
  • To explore the influence of LOX-derived metabolites on skin cancer progression.

Main Methods:

  • Generation of transgenic mouse lines with varying e12S-LOX expression under keratin 6 promoter control.
  • Comparison of skin tumor response in transgenic mice versus wild-type controls.
  • Analysis of LOX isoform expression and metabolite accumulation (e.g., 13S-hydroxyoctadecadienoic acid, 12S-hydroxyeicosatetraenoic acid).

Main Results:

  • Low e12S-LOX expression correlated with decreased tumor response, increased leukocyte-type 12S-LOX, and accumulation of linoleic acid derivatives.
  • High e12S-LOX expression correlated with increased tumor response, keratin 6 promoter-driven upregulation, and accumulation of arachidonic acid derivatives.
  • Demonstrated complex interactions between LOX isoforms and opposing roles of their products in skin carcinogenesis.

Conclusions:

  • e12S-LOX exhibits a complex role in skin carcinogenesis, potentially influenced by expression levels.
  • Linoleic acid and arachidonic acid metabolites derived from LOX activity have opposing effects on skin tumor development.
  • Findings highlight the intricate interplay of LOX pathways in modulating skin cancer progression.

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