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Influences of sphingosine on two-stage skin tumorigenesis in Sencar mice
B Enkvetchakul1, T Barnett, D C Liotta
1Eppley Institute, University of Nebraska Medical Center, Omaha 68198.
Abstract:
Sphingosine (SPH) was studied as an inhibitor of skin tumor promotion in skin cancer initiated by 7,12-dimethylbenz[a]-anthracene (DMBA) and promoted by 12-O-tetradecanoylphorbol-13-acetate (TPA). Two tumorigenesis studies were conducted using female Sencar mice treated with 10 nmol DMBA in 0.2 ml acetone at 8 weeks of age and promoted beginning 1 week later with 3.2 nmol TPA applied twice per week. In the high-dose study, 10 mumol SPH was applied 30 min before each TPA treatment. The low-dose study used 0.5, 0.05, or 0.01 mumol treatments with SPH 30 min before TPA. In the high-dose study SPH treatment alone following initiation by DMBA, and SPH treatment preceding TPA in DMBA-initiated mice accelerated the development of papillomas in comparison with the DMBA/TPA-treated group. The low-dose experiment showed no consistent alteration of tumorigenesis by SPH in the DMBA/TPA-treated groups, and low doses of SPH following DMBA did not promote skin tumorigenesis. SPH treatment did not alter body weight in either experiment.
Insights
Sphingosine (SPH) did not inhibit skin tumor promotion in mice initiated with DMBA and promoted with TPA. High doses of SPH accelerated papilloma development, while low doses showed no consistent effect.
Area of Science:
- Oncology
- Dermatology
- Biochemistry
Background:
- Skin cancer initiation involves carcinogens like DMBA.
- Tumor promotion is often mediated by agents such as TPA.
- Sphingosine (SPH) is a lipid mediator with potential roles in cell signaling.
Purpose of the Study:
- To investigate the role of Sphingosine (SPH) as an inhibitor of skin tumor promotion.
- To evaluate the effects of SPH on skin tumorigenesis initiated by DMBA and promoted by TPA.
Main Methods:
- Two-stage skin tumorigenesis studies were conducted in female Sencar mice.
- Mice were initiated with 7,12-dimethylbenz[a]-anthracene (DMBA) and promoted with 12-O-tetradecanoylphorbol-13-acetate (TPA).
- Varying doses of SPH were administered before TPA treatment.
Main Results:
- High-dose SPH treatment accelerated papilloma development in DMBA-initiated mice.
- Low-dose SPH treatments did not consistently alter tumorigenesis.
- SPH administration did not affect mouse body weight.
Conclusions:
- Sphingosine (SPH) does not act as an inhibitor of skin tumor promotion in this model.
- High concentrations of SPH may potentially promote skin tumorigenesis.
- Further research is needed to elucidate the complex role of SPH in skin cancer.