Vitamin K3 induces antiproliferative effect in cervical epithelial cells transformed by HPV 16 (SiHa cells) through the increase in reactive oxygen species production

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Scharf Santana, Natalia de Carvalho
Lima, Natalia Alves
Desoti, Vania Cristina
Bidoia, Danielle Lazarin
Bonfim Mendonca, Patricia de Souza
Ratti, Bianca Altrao
Nakamura, Tania Ueda
Nakamura, Celso Vataru
Lopes Consolaro, Marcia Edilaine
Ximenes, Valdecir Farias [UNESP]
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Cervical cancer is characterized as an important public health problem. According to latest estimates, cancer of the cervix is the fourth most common cancer among women. Due to its high prevalence, the search for new and efficient drugs to treat this infection is continuous. The progression of HPV-associated cervical cancer involves the expression of two viral proteins, E6 and E7, which are rapidly degraded by the ubiquitin-proteasome system through the increase in reactive oxygen species generation. Vitamins are essential to human substances, participate in the regulation of metabolism, and facilitate the process of energy transfer. Some early studies have indicated that vitamin K3 exerts antitumor activity by inducing cell death by apoptosis through an increase in the generation of reactive oxygen species. Thus, we evaluated the antiproliferative effect and a likely mechanism of action of vitamin K3 against cervical epithelial cells transformed by HPV 16 (SiHa cells) assessing the production of total ROS, the mitochondrial membrane potential, the cell morphology, the cell volume, and the cell membrane integrity. Our results show that vitamin K3 induces an increase in ROS production in SiHa cells, triggering biochemical and morphological events, such as depolarization of mitochondrial membrane potential and decreasing cell volume. Our data showed that vitamin K3 generates an oxidative imbalance in SiHa cells, leading to mechanisms that induce cell death by apoptosis.
Human Papillomavirus, Vitamin K3, Apoptosis SiHa cells
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Archives Of Gynecology And Obstetrics. Heidelberg: Springer Heidelberg, v. 294, n. 4, p. 797-804, 2016.