Skin Cancer 2019: Modified Glucocorticoid as Novel Therapy Model
Posted: Monday, April 8, 2019
Expression of the 11β-hydroxysteroid dehydrogenase type 2 (11βHSD2) protein appears to be increased in non-melanoma skin cancer cells when compared with normal skin cells, according to study results presented at the 2019 World Congress on Advanced Treatments and Technologies in Skin Cancer (Skin Cancer 2019) in Vienna (Poster 2). 11βHSD2 is an enzyme responsible for converting the active corticosteroid, cortisol, to the inactive form, cortisone. Thomas Slaga, PhD, of The University of Texas Health at San Antonio, and colleagues modified the functional group of cortisol at the C-11 position to a fluorine, creating 11-doxyfluorocortisol. This novel cortisol-like compound allowed human cancer cells to overcome the metabolic effect of 11βHSD2.
The researchers studied the effects of 11-doxyfluorocortisol on a panel of normal human epidermal skin cells and skin cancer cell lines PM-1 and Met-4. They found that normal skin cells were more sensitive to glucocorticoid treatment than cancerous PM-1 and Met-4 cells. The potency of 11-doxyfluorocortisol against cell proliferation was comparable to that of cortisol. Additionally, preliminary data suggested that the lipopolysaccharide-induced increase of inflammatory cytokine interleukin-1β was significantly suppressed to a similar extent by cortisol and 11-doxyfluorocortisol.
“The use of 11-doxyfluorocortisol to treat inflammation and cancer, as well as prevent glucocorticoid resistance, is an important area of translation research,” concluded Dr. Slaga and colleagues.
