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The prevalence of head and neck squamous cell carcinoma (HNSCC) has continued to rise for decades. However, drug resistance to chemotherapeutics and relapse, mediated by cancer stem cells (CSCs), remains a significant impediment in clinical oncology to achieve successful treatment. Therefore, we focused on analyzing CSCs in HNSCC and demonstrated the effect of melatonin (Mel) and verteporfin (VP) on SCC‐25 cells. HNSCC CSCs were enriched in the reactive oxygen species‐low state and in sphere‐forming cultures. Combination treatment with Mel and VP decreased HNSCC viability and increased apoptosis without causing significant damage to normal cells. Sphere‐forming ability and stem cell population were reduced by co‐treatment with Mel and VP, while mitochondrial ROS level was increased by the treatment. Furthermore, the expression of mitophagy markers, parkin and PINK1, was significantly decreased in the co‐treated cells. Mel and VP induced mitochondrial depolarization and inhibited mitochondrial function. Parkin/TOM20 was localized near the nucleus and formed clusters of mitochondria in the cells after treatment. Moreover, Mel and VP downregulated the expression of markers involved in epithelial‐mesenchymal transition and metastasis. The migration capacity of cells was significantly decreased by co‐treatment with Mel and VP, accompanied by the down‐regulation of MMP‐2 and MMP‐9 expression. Taken together, these results indicate that co‐treatment with Mel and VP induces mitochondrial dysfunction, resulting in the apoptosis of CSCs. Mel and VP could thus be further investigated as potential therapies for HNSCC through their action on CSCs. [ABSTRACT FROM AUTHOR]

Preeclampsia (PE) is a pregnancy-specific hypertensive syndrome that results in substantial maternal and fetal morbidity and mortality. The exact cause of PE has not been completely elucidate, although abnormal formation of the placenta has been considered. The placenta connects the developing fetus to the uterine wall, producing a large quantity of steroid hormones to maintain pregnancy. Although steroid hormones, particularly progesterone (P4) and estrogen (E2), in the serum of women with PE have been studied, steroidogenesis in the placenta has not well been established. The present study compared the concentrations of steroid hormones, including pregnenolone (PG), P4, dehydroepiandrosterone (DHEA), testosterone (T) and E2, in the serum and placenta of women with PE. PG, P4, DHEA and E2 concentrations tended to be decreased in PE serum and placentas, and the results were statistically significant for P4 and E2 in the serum. Quantification of genes associated with steroidogenesis in the placenta was performed, and the expression of the P4- and E2-synthesizing enzymes testosterone 17-β-dehydrogenase 3 and 3 β-hydroxysteroid dehydrogenase/δ5 4-isomerase type 1 was reduced. Notably, aromatase, an enzyme required for the production of E2, was upregulated in the PE placenta, suggesting that steroidogenic enzymes may be dynamically regulated and may affect the symptoms of PE. In conclusion, the results of the present study suggested that the levels of steroid hormones, including P4 and E2, in the serum and placenta of women with PE are downregulated, which may be mediated by the regulation of steroidogenic enzyme expression in the PE placenta. [ABSTRACT FROM AUTHOR]