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Melatonin-induced KiSS1 expression inhibits triple-negative breast cancer cell invasiveness
1Department of Biotechnology, Korea National University of Transportation, Jeungpyeong, Chungcheongbuk 368-701, Republic of Korea.
Abstract:
Breast cancer is one of the most common types of cancer in women, and its metastasis increases the risk of mortality. Melatonin, a hormone that regulates the circadian rhythm, has been revealed to inhibit breast cancer growth and metastasis. However, its involvement in highly metastatic triple-negative breast cancer cells is yet to be elucidated. The present study demonstrated that melatonin inhibited the metastatic abilities of triple-negative breast cancer cells and prolonged its inhibitory effect via the expression of kisspeptin (KiSS1), which is a suppressor of metastasis. Melatonin at concentrations ranging from 1 nM to 10 µM did not affect the proliferation of metastatic MDA-MB-231 and HCC-70 triple-negative breast cancer cells. However, melatonin repressed invasiveness in triple-negative breast cancer cells. Additionally, conditional medium from melatonin-treated MDA-MB-231 cells repressed the invasiveness of triple-negative breast cancer cells. Melatonin promoted the production of KiSS1, a metastasis suppressor encoded by the KiSS1 gene. In addition, melatonin increased KiSS1 expression via the expression and transcriptional activation of GATA binding protein 3. Silencing of KiSS1 weakened melatonin inhibition of breast cancer cell invasiveness. Therefore, the present study concluded that melatonin activates KiSS1 production in metastatic breast cancer cells, suggesting that melatonin activation of KiSS1 production may regulate the process of breast cancer metastasis.
Insights
Melatonin, a circadian rhythm hormone, inhibits triple-negative breast cancer metastasis by increasing kisspeptin (KiSS1) expression. This hormone activation of KiSS1 production offers a potential therapeutic strategy for breast cancer metastasis.
Area of Science:
- Oncology
- Endocrinology
- Molecular Biology
Background:
- Breast cancer metastasis significantly increases mortality risk.
- Melatonin, a circadian rhythm hormone, shows potential in inhibiting cancer growth and metastasis.
- The role of melatonin in highly metastatic triple-negative breast cancer (TNBC) requires further investigation.
Purpose of the Study:
- To investigate the effect of melatonin on the metastatic abilities of triple-negative breast cancer cells.
- To elucidate the underlying molecular mechanisms, particularly the role of kisspeptin (KiSS1), in melatonin's action.
- To determine if melatonin influences KiSS1 expression and its impact on metastasis.
Main Methods:
- Treatment of MDA-MB-231 and HCC-70 triple-negative breast cancer cells with varying melatonin concentrations (1 nM to 10 µM).
- Assessment of cell invasiveness and proliferation.
- Analysis of KiSS1 gene and protein expression, including the role of GATA binding protein 3.
- Conditional medium experiments and KiSS1 silencing studies.
Main Results:
- Melatonin did not affect the proliferation of TNBC cells but significantly repressed their invasiveness.
- Melatonin treatment increased KiSS1 production and expression in TNBC cells.
- Melatonin enhanced KiSS1 expression through GATA binding protein 3 activation.
- Silencing KiSS1 diminished the inhibitory effect of melatonin on breast cancer cell invasiveness.
Conclusions:
- Melatonin inhibits the metastatic potential of triple-negative breast cancer cells.
- Melatonin activates KiSS1 production, a key metastasis suppressor, in these cells.
- The melatonin-mediated activation of KiSS1, potentially via GATA3, suggests a novel regulatory pathway for breast cancer metastasis.
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