Breast cancer therapy based on melatonin.
Study Goal
The researchers aimed to evaluate melatonin's potential in breast cancer therapy, focusing on its SERM and SEEM properties and the impact of light-at-night on melatonin suppression.
Results Summary
Melatonin demonstrated oncostatic properties by modulating estrogen-regulated cell proliferation and enzyme activity, with effects mediated by MT1 receptors. Light-at-night suppressed melatonin production, increasing breast cancer risk, while filtering blue light was proposed to mitigate this risk.
Population
Primarily focused on breast cancer cells expressing ERα and rat mammary tumors; epidemiologic studies included women exposed to light-at-night.
Effective Dosage
Physiologic doses (specific amounts not provided)
Duration
Not specified
Interactions
None mentioned
| Intervention | Direction | Endpoint | Population | Dosage | Impact | Claim # |
|---|---|---|---|---|---|---|
melatonin and melatoninergic drugs | neutral | Selective Estrogen Receptor Modulator (SERM) and Selective Estrogen Enzyme Modulator (SEEM) properties | - | - | usefulness in breast cancer therapy is based on | #1 |
melatonin | neutral | oncostatic properties | - | - | has | #2 |
nocturnal suppression by light-at-night (LAN) | increase | breast cancer | - | - | has been considered a risk-factor for | #3 |
melatonin | neutral | estrogen-regulated cell proliferation, invasiveness and expression of proteins, growth factors and proto-oncogenes (hTERT, p53, p21, TGFβ, E-cadherin, etc.) | cells expressing ERα | - | modulation of | #4 |
melatonin | decrease | P450 aromatase, estrogen sulfatase and type 1, 17β- hydroxysteroid dehydrogenase | - | - | acts like a SEEM, inhibiting expression and activity of | #5 |
melatonin | increase | estrogen sulfotransferase | - | - | acts like a SEEM, stimulating that of | #6 |
LAN | increase | rat mammary tumors | rat | - | enhances the growth of | #7 |
LAN | decrease | melatonin production | rat | - | decreasing or suppressing | #8 |
exposure to LAN | increase | breast cancer risk | women | - | increased | #9 |
wavelength light of the blue spectral region | decrease | nocturnal melatonin | - | - | causes the strongest suppression of | #10 |
The usefulness of melatonin and melatoninergic drugs in breast cancer therapy is based on its Selective Estrogen Receptor Modulator (SERM) and Selective Estrogen Enzyme Modulator (SEEM) properties. Because of the oncostatic properties of melatonin, its nocturnal suppression by light-at-night (LAN) has been considered a risk-factor for breast cancer. Melatonin's SERM actions include modulation of estrogen-regulated cell proliferation, invasiveness and expression of proteins, growth factors and proto-oncogenes (hTERT, p53, p21, TGFβ, E-cadherin, etc.). These actions are observable with physiologic doses of melatonin only in cells expressing ERα, and mediated by MT1 melatonin receptors. Melatonin acts like a SEEM, inhibiting expression and activity of P450 aromatase, estrogen sulfatase and type 1, 17β- hydroxysteroid dehydrogenase, but stimulating that of estrogen sulfotransferase. This double action mechanism (SERM and SEEM), and the specificity for ERα bestows melatonin with potential advantages for breast cancer treatments, associated with other antiestrogenic drugs, and idea already patented. LAN enhances the growth of rat mammary tumors by decreasing or suppressing melatonin production. Epidemiologic studies have also described increased breast cancer risk in women exposed to LAN. Since the strongest suppression of nocturnal melatonin occurs with wavelength light of the blue spectral region, optical and lightening devices filtering the blue light spectrum have been proposed to avoid the risks of light-induced suppression of nocturnal melatonin.